bims-fibdiv Biomed News
on Fibroblast diversity
Issue of 2025–12–28
29 papers selected by
Emilio Ernesto Méndez Olivos, University of Calgary



  1. Front Pharmacol. 2025 ;16 1678953
      Keloids and hypertrophic scars (HTS) represent aberrant wound healing characterized by excessive fibroblast activity and extracellular matrix accumulation. The PI3K/AKT/mTOR signaling pathway is vital in regulating these processes, promoting fibroblast proliferation, survival, and collagen synthesis. Dysregulation of this pathway, driven by genetic mutations, post-transcriptional modulation, and upstream signaling, contributes significantly to the pathogenesis of pathological scarring. This review collects current knowledge on the molecular mechanisms underlying PI3K/AKT/mTOR activation in keloids and HTS, highlighting the roles of key regulators such as PTEN, NEDD4, and non-coding RNAs. It also evaluates therapeutic strategies targeting this axis, including small-molecule inhibitors, natural compounds, and emerging delivery platforms. Targeting PI3K/AKT/mTOR offers a compelling avenue for developing effective, mechanism-based keloid and hypertrophic scarring treatments. The PI3K/AKT/mTOR signaling axis is central to these cellular mechanisms, which drive fibroblast proliferation, survival, myofibroblast transdifferentiation, and metabolic reprogramming (including suppressed autophagy and enhanced glycolysis.
    Keywords:  PI3K/Akt/mTOR pathway; drug delivery platforms; extracellular matrix; fibroblast proliferation; hypertrophic scar; keloid; non-coding RNAs; targeted therapy
    DOI:  https://doi.org/10.3389/fphar.2025.1678953
  2. 3 Biotech. 2026 Jan;16(1): 32
      Liver fibrosis is a progressive pathological condition characterised by excessive deposition of extracellular matrix components, primarily driven by chronic liver injury and activation of hepatic stellate cells. This pathological remodelling disrupts hepatic architecture and function, and if left untreated, may advance to cirrhosis, liver failure, or hepatocellular carcinoma, a major contributor to global morbidity and mortality. Flavonoids are a diverse group of polyphenolic compounds found in plants, known for their antioxidant, anti-inflammatory, antiviral, and hepatoprotective properties. Their beneficial effects on liver health have been widely explored in preclinical and clinical studies. Apigenin (4',5,7-Trihydroxyflavone) is a naturally occurring flavonoid (specifically a flavone) widely distributed in fruits, vegetables, and herbs, especially in parsley, celery, chamomile, and oranges. It has gained significant scientific attention due to its antioxidant, anti-inflammatory, neuroprotective, and hepatoprotective properties. Preclinical studies demonstrate that apigenin mitigates fibrogenesis by attenuating oxidative stress, suppressing pro-inflammatory cytokine production, and inhibiting HSC activation. Mechanistically, it modulates multiple signalling pathways and molecular targets such as TGF-β1/Smad, NF-κB, PI3K/AKT, PPARα, GSK3β, MAPK, MLKL, Nrf-2/Keap1, and NLRP3 inflammasome, thereby exerting a multitargeted antifibrotic response. Furthermore, apigenin's ability to restore redox homeostasis and regulate apoptotic signalling underscores its therapeutic potential. Considering the potential of apigenin in modulating these mediators, the present study was conceptualised to study the mechanistic interplay underlying its anti-fibrotic effects. By investigating these interconnected pathways, this study will provide foundational insights that will enable future researchers to address existing gaps and further elucidate apigenin's potential in liver fibrosis.
    Keywords:  Apigenin; Liver fibrosis; Nrf-2; PPARα; TGF-β/Smads
    DOI:  https://doi.org/10.1007/s13205-025-04641-7
  3. J Cell Physiol. 2025 Dec;240(12): e70112
      Idiopathic pulmonary fibrosis (IPF) is an incurable lung disease that ultimately terminates in death or lung transplantation. It is characterized by a restrictive pattern with impaired diffusion capacity, and typically presents with repeated acute exacerbations that result in permanent and progressive loss of respiratory function. IPF bears complicated and likely multifactorial etiology manifesting in the dysfunction of multiple cell types, a 2-year mortality over 40%, and available treatments can only slow disease progression. Distinct metabolic disturbances in IPF underscore the mechanisms of deranged cell function, including regional oxidative stress, fibrotic extracellular matrix production, and epithelial dysfunction including impaired pulmonary surfactant production. Although the precise profile of metabolic derangements in IPF remain contentious across multiple studies and models of disease, metabolism represents a critically untapped pathway for therapeutic intervention. In this review, the mechanisms underlying IPF development and progression are isolated and linked to cell-specific alterations in metabolic function. We furthermore compare various in vivo and in vitro models of IPF with focus on metabolic analyses, and critically compare them to patient-derived data. Finally, new metabolically-associated biomarkers of IPF progression are discussed, and recommendations for further IPF modeling and metabolic targeting of IPF-related processes are provided. This review serves to provide a consensus survey of the current metabolomic IPF landscape, as well as a critical discussion of next steps for in vitro modeling to develop disease-modifying therapeutics targeting dysregulated metabolism in IPF.
    Keywords:  alveoli; epithelium; fibroblast; glycolysis; immune; inflammation; interstitial lung disease; macrophage; restrictive lung disease
    DOI:  https://doi.org/10.1002/jcp.70112
  4. J Pathol. 2025 Dec 23.
      Chronic kidney disease (CKD) is a major global health challenge affecting over 10% of the adult population. A hallmark of CKD progression is the transdifferentiation of kidney fibroblasts into extracellular matrix-producing myofibroblasts, a key mechanism involved in the decline of kidney function and the development of kidney failure. Fibroblasts maintain the structural integrity of the kidney and support epithelial survival, repair, and regeneration after acute kidney injury. Maladaptive repair is a failure to resolve fibroblast activation, which ultimately progresses to chronic injury and CKD. In this study, we showed that the membrane-bound coreceptor neuropilin 1 (NRP1) was essential to maintain fibroblast function and prevent their transdifferentiation into myofibroblasts. We used the myelin protein zero-Cre (P0-Cre) to specifically abrogate Nrp1 in kidney resident fibroblasts during fibrosis progression. We employed kidney-induced interstitial fibrosis models combined with a lineage-tracing strategy, single-cell RNA sequencing analysis, and ex vivo explant cultures to reveal a cell autonomous protective role for NRP1 in limiting fibrosis. Furthermore, we extended the analysis by showing that Nrp1 conditional mutants were more prone to develop cardiac fibrosis in a mouse model of heart failure. Collectively, these findings provide new insights into the signalling pathways controlling the transition from acute to chronic kidney disease conversion and identify NRP1 as a novel regulator of fibroblast supportive function. © 2025 The Author(s). The Journal of Pathology published by John Wiley & Sons Ltd on behalf of The Pathological Society of Great Britain and Ireland.
    DOI:  https://doi.org/10.1002/path.70009
  5. Bull Math Biol. 2025 Dec 26. 88(1): 13
      Understanding the interactions between cells and the extracellular matrix (ECM) during collective cell invasion is crucial for advancements in tissue engineering, cancer therapies, and regenerative medicine. This study focuses on the roles of contact guidance and ECM remodelling in directing cell behaviour, with a particular emphasis on exploring how differences in cell phenotype impact collective cell invasion. We present a computationally tractable two-dimensional hybrid model of collective cell migration within the ECM, where cells are modelled as individual entities and collagen fibres as a continuous tensorial field. Our model incorporates random motility, contact guidance, cell-cell adhesion, volume filling, and the dynamic remodelling of collagen fibres through cellular secretion and degradation. Through a comprehensive parameter sweep, we provide valuable insights into how differences in the cell phenotype, in terms of the ability of the cell to migrate, secrete, degrade, and respond to contact guidance cues from the ECM, impacts the characteristics of collective cell invasion.
    DOI:  https://doi.org/10.1007/s11538-025-01560-9
  6. Front Bioeng Biotechnol. 2025 ;13 1710978
      As the fundamental environment for cell survival, the extracellular matrix (ECM) not only serves as the substrate for cell function and structure formation but also guides cell activities through its dynamic physical properties. Therefore, the relationships by which the physical and mechanical properties of the ECM guide cell behavior such as growth, development, differentiation and reproduction are important to understand. Because substrate stiffness is an important physical property that influences cell behavior, this paper focuses on the relationship between stiffness and cell behavior. Hydrogels, as networks of hydrophilic polymer chains, are an excellent model for the physical properties of the ECM in cellular studies due to its multiple similarities with the ECM. This review classifies hydrogels in terms of their origin and their relative stiffness and presents an overview of their formation, properties, regulation, and applications. We believe that hydrogels with variable elastic moduli will continue to be of considerable use in future studies to further elucidate the effects of mechanical cues on cell behavior.
    Keywords:  cell behavior; extracellular matrix; hydrogel; tissue engineering; tunable stiffness
    DOI:  https://doi.org/10.3389/fbioe.2025.1710978
  7. bioRxiv. 2025 Dec 10. pii: 2025.12.08.692836. [Epub ahead of print]
      Fibrotic scarring is a pervasive and unresolved challenge in medicine, leading to permanent disfigurement, impaired mobility, and severe disruption of basic skin functions including elasticity, barrier protection, and thermoregulation. Despite its far-reaching personal, clinical, and economic impact, affecting hundreds of millions worldwide after surgery, trauma, and burns, no effective treatments exist to halt or reverse pathological scar formation. Scarring results from uncontrolled TGF-b1 signaling, which drives excessive deposition of extracellular matrix (ECM) proteins such as collagen-I/III and accumulation of alpha-smooth muscle actin (alpha-SMA), producing rigid, dysfunctional tissue. Here, we present a mechanistically guided approach targeting this unmet clinical need, leveraging the natural antifibrotic peptide hormone relaxin-2 (RLX-2) to actively remodel dermal architecture. RLX-2 signals via its G-protein coupled receptor RXFP1, upregulating matrix metalloproteinases (MMPs) and inhibiting aberrant ECM production. In TGF-b1-activated dermal fibroblasts across 2D and 3D in vitro models, ex vivo healthy and scarred human skin samples - cultured under physiological and pathological tension - and in an in vivo murine burn wound model, RLX-2 robustly suppresses fibrosis, restores regenerative tissue features, and rescues dermal architecture. Importantly, RLX-2 achieves this result without compromising the normal wound healing process, highlighting its potential as a transformative therapy for both prevention and reversal of pathological scarring.
    DOI:  https://doi.org/10.64898/2025.12.08.692836
  8. Ann Med. 2026 Dec;58(1): 2603022
       BACKGROUND/OBJECTIVES: As a pivotal mechanosensitive ion channel, Piezo-type mechanosensitive ion channel component 1 (Piezo1) converts mechanical stimuli into biochemical signals that regulate key oncogenic processes, including tumour cell proliferation, migration and invasion. Emerging evidence demonstrates that Piezo1 is widely expressed across various cellular compartments of the tumour microenvironment (TME), and its elevated expression strongly correlates with adverse clinical outcomes. A comprehensive understanding of the complex interactions between Piezo1 activation and cytokine networks in different TME cell populations is therefore essential for developing innovative and effective anti-tumour therapeutic strategies. In this review, we aimed to highlight the molecular mechanisms of Piezo1, systematically elucidating how the mechanical stimulation-Piezo1 signalling pathway within the TME contributes to tumour immune escape and malignant progression. Furthermore, we summarized current research advances in Piezo1-targeting drugs and clinical trials, and discuss strategies to improve tissue specificity while minimizing off-target effects.
    DISCUSSION: A comprehensive literature review was conducted, focusing on the specific mechanisms through which Piezo1 regulates endothelial cells, immune cells, cancer-associated fibroblasts and the extracellular matrix within the TME. Activation of Piezo1 in endothelial and immune cells promotes tumour angiogenesis and immune evasion.
    CONCLUSION: Piezo1 plays a critical role in tumour progression and represents a promising therapeutic target for cancer treatment.
    Keywords:  Piezo1; TME; immunotherapy; mechanical signals; tumour progression
    DOI:  https://doi.org/10.1080/07853890.2025.2603022
  9. Eur J Pharmacol. 2025 Dec 24. pii: S0014-2999(25)01258-0. [Epub ahead of print] 178504
      Mulberry (Morus nigra L.) is traditionally recognized for its bone-strengthening properties, yet its active constituents and underlying mechanisms remain incompletely understood. This study investigates the effects of maclurin, a key flavonoid from mulberry, on extracellular matrix (ECM) deposition and bone formation. In vitro, maclurin (5-20 μM) treatment enhanced ECM protein expression, including fibronectin (FN), laminin subunit gamma-2, and collagen alpha-1(I) chain (Col I) in MC3T3-E1 osteoblasts in a dose-dependent manner. Transcriptomic analysis suggested the involvement of PI3K/Akt signalling pathway, which was subsequently validated by increased Akt phosphorylation that was reversed by siAkt and PI3K inhibitor LY294002. In a subcutaneous ectopic bone formation model, oral maclurin administration (0.5-2.0 mg/kg) promoted Col I and FN expressions, improved collagen fibre organization, and increased calcium deposition in newly formed bone tissues. These results provide experimental evidence for osteogenic activity of maclurin and enhance our understanding of the bone-health benefits associated with mulberry.
    Keywords:  PI3K/Akt pathway; bone formation; extracellular matrix; maclurin; transcriptome
    DOI:  https://doi.org/10.1016/j.ejphar.2025.178504
  10. Front Pharmacol. 2025 ;16 1734449
       Background: Liver fibrosis (LF) is a progressive condition that can advance to cirrhosis and liver failure, posing a major global health burden. Hepatic stellate cells (HSCs) are central to LF pathogenesis via extracellular matrix (ECM) production and inflammatory regulation, and have been widely explored as therapeutic targets.
    Methods: We searched the Web of Science Core Collection (WoSCC), Scopus, and PubMed for English-language publications using the keywords "liver fibrosis" and "stellate cells." Additionally, ClinicalTrials.gov was queried for clinical trials, and the Innojoy search engine was used for patents. Analyses were performed using CiteSpace (version 6.2.R4), VOSviewer, R, and Microsoft Excel to examine publication trends, collaboration and citation structures, keyword co-occurrence, clustering, citation bursts, and International Patent Classification (IPC) profiles.
    Results: From 2000 to 2025, annual publications increased from 3 to 50 (≈16.7-fold), totaling 1,042 papers; China led output (n = 672), followed by the United States (n = 162), spanning hepatology and pharmacology. Thirteen thematic clusters were identified across etiology, molecular mechanisms, and therapeutics/delivery, with targeted delivery and intervention emerging as the leading frontier. Burst terms highlighted sustained reliance on rodent in vivo models (rats/mice; carbon tetrachloride injury) alongside hepatocellular carcinoma-related signals. The patent landscape was dominated by therapeutic-use and small-molecule classes (A61P 1/16; A61K 31/), with expansion to specialized dosage forms and combination regimens (A61K 9/00; A61K 45/06) and multimodal platforms involving nucleic acids (C12N 15/113) and antibodies (C07K 16/18). Clinical trials shifted from early small molecule monotherapies to more diversified, combinable regimens.
    Conclusion: Integrating bibliometrics with patent and clinical landscapes, this study delineates an evolution from mechanism discovery to precision intervention in HSC - focused LF research. Future priorities include improving target/tissue specificity and advancing multimodal, patient stratified strategies to enhance translational efficiency.
    Keywords:  anti-fibrotic therapy; bibliometrics; clinical trials; hepatic stellate cells; liver fibrosis; patents; targeted delivery
    DOI:  https://doi.org/10.3389/fphar.2025.1734449
  11. Mater Today Bio. 2025 Dec;35 102640
      Immunoregulatory properties of guided bone regeneration (GBR) membranes are essential for modulating the osteoimmune microenvironment to enhance osteogenesis. Decellularized amnion membrane (DAM), an extracellular matrix material derived from the placenta through the removal of cells and antigenic components, has attracted attention due to its low immunogenicity and rich composition. This study investigated the role of DAM in modulating the immune microenvironment, its impact on osteogenesis, and associated mechanisms during the GBR process. DAM exhibited high biocompatibility and directly promoted osteogenesis in vitro. Furthermore, DAM induced macrophage M2 polarization, mitigated oxidative stress under inflammatory contexts, and optimized the immune microenvironment, thereby indirectly enhancing cell migration and osteogenic differentiation. Multi-omics analysis revealed a crucial role of the PI3K-Akt signaling pathway, coordinated with immune-related TLR and TNF signaling pathways, in this process-highlighting the potential applications of DAM in the treatment of inflammatory bone defects. DAM's abundant bioactive components and distinctive three-dimensional architecture enable this synergistic effect. In vivo, DAM effectively inhibited inflammation and accelerated bone regeneration in a rat model of critical-size cranial defects. This study demonstrates that DAM possesses strong osteoimmunomodulatory properties and elucidates its underlying mechanisms in bone regeneration, making it a promising GBR membrane for clinical applications.
    Keywords:  Decellularized amnion membrane; Guided bone regeneration; Osteogenic differentiation; Osteoimmunomodulatory
    DOI:  https://doi.org/10.1016/j.mtbio.2025.102640
  12. Bioorg Chem. 2025 Dec 15. pii: S0045-2068(25)01274-X. [Epub ahead of print]169 109394
      Hepatic fibrosis is a central pathological feature of chronic liver diseases, but effective pharmacological interventions remain limited. Protopine (PTP), a naturally isoquinoline alkaloid compound, has been reported to exhibit anti-inflammatory and hepatoprotective properties. However, its specific role and mechanisms in hepatic fibrosis remain unclear. This study employed a CCl4-induced murine model and a TGF-β1-stimulated LX-2 cell model to investigate the therapeutic effects and molecular mechanisms of PTP in hepatic fibrosis. The results demonstrated that PTP significantly alleviated liver injury and collagen deposition, suppressed hepatic stellate cell (HSC) activation and restored extracellular matrix (ECM) homeostasis. Mechanistically, PTP directly binds to histone deacetylase 6 (HDAC6) and downregulated the expression of NLRP3 and α-SMA at the mRNA and protein levels, reducing the secretion of downstream pro-inflammatory factors IL-1β and IL-18. Further use of an HDAC6 inhibitor confirmed the consistent effect with PTP. These findings reveal that PTP exerts anti-fibrotic effects through the HDAC6-NLRP3 signaling axis, providing a theoretical basis for its development as a lead compound for the treatment of hepatic fibrosis.
    Keywords:  HDAC6; Hepatic fibrosis; Hepatic stellate cells; NLRP3; Protopine
    DOI:  https://doi.org/10.1016/j.bioorg.2025.109394
  13. Int Immunopharmacol. 2025 Dec 21. pii: S1567-5769(25)02081-8. [Epub ahead of print]170 116092
      Copper (Cu)-dependent aggregation of lipoylated proteins in mitochondria triggers cuproptosis, a newly discovered modality of regulated cell death marked by impaired mitochondrial respiration. During the progression of hepatic fibrosis (HF), hepatocytes, responsible for Cu storage and metabolism, exhibit vigorous mitochondrial activity and are supposed to be cuproptosis-susceptible. However, the cellular landscape of cuproptosis in fibrotic livers remains unclear, and the therapeutic potential of cuproptosis suppression in resolving HF has yet to be explored. In this study, single-cell RNA sequencing data from mouse models and clinical samples from HF patients show that hepatocytes are the dominant cell population attacked by cuproptosis. These cuproptotic hepatocytes release pro-fibrotic signals that activate hepatic stellate cells (HSCs), inducing the formation of fibrotic scar. Tannic acid (TA), a polyphenolic-molecule cuproptosis inhibitor, can combat the changes in cuproptotic hepatocytes stimulated by elesclomol plus Cu supplement in vitro, including intracellular Cu (I) concentration, mitochondrial membrane potential, and expression pattern of cuproptosis regulators. In addition, the production of pro-fibrotic signals is inhibited by TA, and subsequently the activation of HSCs. Finally, TA is demonstrated to prevent the progression of HF in mouse models, as evidenced by the improvement of liver architecture and function. Proteomic analysis reveals that the disturbed lipid metabolism and cuproptosis regulator expression in fibrotic livers are both rescued by TA. Collectively, these findings highlight hepatocyte cuproptosis as a key driver of the fibrotic process, and its suppression holds great therapeutic promise for treating HF.
    Keywords:  Cuproptosis; Hepatic fibrosis; Hepatocytes; Tannic acid
    DOI:  https://doi.org/10.1016/j.intimp.2025.116092
  14. Sci Rep. 2025 Dec 24.
      The extracellular matrix (ECM) is an expansive network of polymers that regulates cell adhesion, migration, and tissue morphogenesis, and that becomes dysregulated in fibrotic disease states. Of the many ECM proteins, fibronectin (FN) is foundational and FN fibrils are instrumental in promoting deposition of many other ECM proteins. FN fibrils form by cell receptor-mediated polymerization of secreted FN dimers. To provide a deeper understanding of the FN assembly process, we sought to identify FN-binding peptides that could be used to target FN during matrix assembly. Here we report the isolation of a FN-binding peptide, S2, by M13 phage display. When displayed within a GST-S2-EGFP fusion protein, S2 directs incorporation of the fluorescent fusion protein into FN fibrils during fibroblast matrix assembly, enabling direct visualization of fibril formation and accumulation. The S2 fusion protein remains stably associated with FN in decellularized matrices. Live cell imaging with GST-S2-EGFP revealed events in matrix formation and maturation and highlighted distinct features of FN assembly such as nascent fibril nucleation and elongation from coalescing FN aggregates. This S2 peptide fusion protein represents a new tool for real-time analysis of the ECM, for generation of fluorescent scaffolds, and for directing functional proteins to FN matrix.
    Keywords:  Extracellular matrix; Fibronectin; GFP fusion protein; Live-imaging; Matrix assembly; Phage display
    DOI:  https://doi.org/10.1038/s41598-025-33556-9
  15. J Biomed Res. 2025 Dec 25. 1-15
      Abdominal aortic aneurysm (AAA) is a life-threatening vascular disorder characterized by localized dilation of the abdominal aorta and a high mortality rate once rupture occurs. At present, therapeutic approaches for AAA are primarily confined to operative repair. Thus, a comprehensive understanding of its pathogenesis is crucial for the development of novel pharmacological interventions. Although the underlying mechanisms remain incompletely defined, several critical pathological features have been identified, including inflammation, extracellular matrix degradation, and loss of vascular smooth muscle cells. In recent years, perivascular adipose tissue (PVAT), an active endocrine and paracrine organ surrounding blood vessels, has emerged as an essential regulator of various cardiovascular diseases. PVAT has been shown to remodel the extracellular matrix and influence vascular smooth muscle cell behavior by establishing a pro-inflammatory milieu, thereby affecting the structural integrity and reactivity of the arterial wall. This review summarizes recent research advances in PVAT-driven inflammation in AAA and highlights the translational potential for clinical applications, aiming to provide new insights for future research.
    Keywords:  abdominal aortic aneurysm; adipokine; adipose tissue; inflammation; perivascular adipose tissue
    DOI:  https://doi.org/10.7555/JBR.39.20250415
  16. FASEB J. 2025 Dec 31. 39(24): e71368
      Chronic wounds, a major healthcare burden, are characterized by impaired fibroblast function and ECM remodeling. Thrombospondin-2 (TSP2), a matricellular glycoprotein, has been shown to negatively regulate wound healing. Here, we investigated the cellular and transcriptomic consequences of TSP2 deficiency in dermal fibroblasts, key cells in tissue repair and extracellular matrix (ECM) remodeling. Using bulk RNA sequencing of wild-type (WT) and TSP2 knockout (TSP2 KO) murine primary fibroblasts, we identified upregulation of pro-regenerative molecules and signaling pathways, specifically TGF-β3 and Wnt4/β-catenin, in the latter. To overcome the inherent variability of primary cells and establish a robust model, we generated a stable CRISPR/Cas9-engineered TSP2 knockout in NIH3T3 fibroblasts. This system confirmed that TSP2 depletion enhances fibroblast proliferation and migration, associated with increased activity of TGF-β3 and Wnt/β-catenin signaling pathways. These findings not only provide novel mechanistic insights into the role of TSP2 in regulating fibroblast function and ECM interactions during tissue repair, but also highlight TSP2 as a potential therapeutic target for promoting regeneration in healing-impaired or chronic wounds.
    Keywords:  Wnt/β‐catenin; extracellular matrix; fibroblasts; thrombospondin‐2; transforming growth factor beta
    DOI:  https://doi.org/10.1096/fj.202501884R
  17. Free Radic Biol Med. 2025 Dec 22. pii: S0891-5849(25)01450-9. [Epub ahead of print]
       BACKGROUND: Systemic sclerosis (SSc), or scleroderma, is an autoimmune disease with localized/diffuse skin thickening and fibrosis as main features, where disease progression links to inflammatory immunity. Although atorvastatin has anti - inflammatory effects, its role in skin fibrosis is unclear. This study aimed to explore atorvastatin's anti - inflammatory and antifibrotic effects and mechanisms.
    METHODS: In vivo, the anti - inflammatory and anti - fibrotic effects of atorvastatin were evaluated using a bleomycin - induced experimental SSc model and a keloid xenograft model. In vitro, an LPS - induced macrophage polarization model and a TGF - β1 - induced fibroblast activation model were employed for research. 16S rRNA sequencing was conducted to study the skin surface microbiota. To explore the mechanism of action of atorvastatin, methods such as drug affinity reaction target stability technology, molecular docking, and microcalorimetry experiments were adopted.
    RESULTS: Atorvastatin alleviated skin fibrosis, reduced thickness, collagen deposition, and macrophage aggregation in mouse models. In vitro, it inhibited macrophage and fibroblast activation. It also improved skin bacteria at the genus level. CD14 was confirmed as a direct target of atorvastatin, and atorvastatin inhibited LPS - TLR4 binding.
    CONCLUSIONS: CD14 is a potential therapeutic target for SSc skin fibrosis, and atorvastatin may be a new treatment option.
    Keywords:  Atorvastatin; CD14; SSc; fibrosis; macrophage
    DOI:  https://doi.org/10.1016/j.freeradbiomed.2025.12.033
  18. Arthritis Rheumatol. 2025 Dec 26.
       OBJECTIVES: Localized scleroderma (LoS) and systemic sclerosis (SSc) are both fibrotic diseases, but LoS is limited to the skin, whereas SSc involves systemic organ fibrosis. This study aimed to elucidate the mechanisms underlying these differences.
    METHODS: Skin biopsies from 3 healthy controls, 3 patients with LoS, and 3 patients with SSc underwent immunofluorescence and single-cell RNA sequencing (scRNA-seq). Key molecular functions were validated using in vitro assays and murine models.
    RESULTS: Immunofluorescence revealed a high prevalence of tertiary lymphoid structures (TLS) in LoS lesions (65.7%) compared to SSc (14.3%, p = 0.0013). scRNA-seq identified T follicular helper (Tfh) cells enriched within TLS in LoS. Tfh cells likely promote B cell recruitment via the CXCL13/CXCR5 axis, and integrin α4 may support Tfh cell retention, contributing to TLS stability. These organized immune aggregates, together with elevated TGF-β expression, may drive localized fibroblast activation and skin fibrosis in LoS. In contrast, SSc lesions contained fibroblasts with high CREB3L1 expression. CREB3L1 overexpression increased type I collagen, fibronectin 1, and periostin levels in fibroblasts, while knockdown reduced them. In a SSc mouse model, CREB3L1 upregulation worsened skin and lung fibrosis, whereas knockdown alleviated it.
    CONCLUSION: These findings suggest that LoS fibrosis is driven by TLS-mediated local immune activation, whereas the systemic activation of CREB3L1-expressing fibroblasts plays an important role in SSc fibrosis. Targeting local inflammation may benefits LoS, while targeting CREB3L1 offers a promising antifibrotic strategy in SSc.
    DOI:  https://doi.org/10.1002/art.70039
  19. In Vitro Cell Dev Biol Anim. 2025 Dec 22.
      Diabetic nephropathy (DN) is a critical complication of diabetes mellitus. Icariside II, a bioactive compound from epimedium, is known for its anti-hyperglycemic properties, but its mechanism in DN remains unclear. Our study aimed to explore Icariside II's protective effects against high-glucose (HG) induced podocytes injury using an in vitro model. We assessed cell viability and proliferation using the CCK8 assay after treating cells with Icariside II. qPCR and Western blot analysis were used to measure the mRNA and protein expressions of DNMT1, α-SMA, fibronectin and collagen IV. Molecular docking studies were performed using DNMT1's 3D structure from the Protein Data Bank. DNMT1 overexpression levels were quantified via qRT-PCR and western blot. Immunofluorescence staining and ELISA assays evaluated TGF-β1, inflammatory cytokines, respectively. GSH, MDA, and intracellular Fe2+ were measured using biochemical assay kits and FerroOrange probes, respectively. Western blot analysis was used to measure the protein expressions of GPX4, SLC7A11, ACSL4 and TFR1. Results showed Icariside II inhibits HG induced proliferation, inflammation and extracellular matrix (ECM) accumulation in MPC-5 cells. Besides, Icariside II also reduced inflammation, ECM accumulation and ferroptosis by downregulating DNMT1. However, the intervention treatment with Ferrostatin-1 could effectively counteract this effect. Icariside II mitigated HG-induced inflammation and ECM accumulation by down-regulating DNMT1 and ferroptosis.
    Keywords:  DNMT1; Diabetic nephropathy; Ferroptosis; Icariside II; Podocyte
    DOI:  https://doi.org/10.1007/s11626-025-01142-y
  20. Front Immunol. 2025 ;16 1725948
      Cholangiocarcinoma (CCA) is a highly invasive malignant tumor of the biliary tract, and its detection is commonly delayed until advanced stages owing to a lack of early symptoms, with dismal overall survival and a high propensity for chemoresistance. CCA is primarily classified based on its anatomical location, encompassing distinct molecular subtypes with both intertumoral and intratumoral heterogeneity. Beyond malignant epithelial cells, CCA harbors a complicated and dynamically evolving tumor microenvironment (TME), in which multiple stromal cell types orchestrate disease progression through intricate crosstalk networks. Among them, cancer-associated fibroblasts(CAFs) constitute the numerically predominant cellular component in the matrix of CCA, playing pivotal roles in extracellular matrix remodeling, immune regulation, angiogenesis, and metastasis. Traditionally regarded as predominantly tumor-promoting, CAFs have recently been recognized as a heterogeneous population with transcriptionally and functionally distinct subsets, some of which may even exert tumor-suppressive functions. Deciphering the complex biology of CAFs is crucial for advancing CCA therapy. This review provides a thorough examination of the origins, functions, and pro-tumorigenic mechanisms of CAFs in the CCA TME, alongside a critical evaluation of advancements and obstacles in the development of therapies targeting CAFs.
    Keywords:  cancer-associated fibroblasts; cholangiocarcinoma; heterogeneity; interactions; targeted therapy
    DOI:  https://doi.org/10.3389/fimmu.2025.1725948
  21. Sci Rep. 2025 Dec 26.
      Calcific aortic valve disease currently lacks effective treatments beyond aortic valve replacement, largely due to an incomplete understanding of its pathogenesis. Emerging evidence suggests that the gut microbiome influences cardiovascular health through the production of metabolites derived from dietary components. Among these metabolites, trimethylamine-N-oxide (TMAO) has been identified as a potential causal factor for several cardiovascular conditions. However, its specific role in the development of aortic valve disease remains poorly understood. This study sought to investigate the impact of TMAO on valvular interstitial cells (VICs), the most abundant cell type in the aortic valve. Here, we demonstrate that TMAO activates aortic VICs towards a myofibroblastic phenotype through the induction of endoplasmic reticulum stress. Using a novel in vitro protocol to generate quiescent VICs, we found that TMAO induces the upregulation of the myofibroblastic proteins α-smooth muscle actin and transgelin in a sex-independent manner. These quiescent VICs were more sensitive to TMAO than conventionally cultured VICs. Treatment with TMAO also elevated extracellular matrix production and oxidative stress, phenotypic hallmarks of an activated profibrotic state. Finally, inhibition of the endoplasmic reticulum stress kinase prior to TMAO treatment blocked all effects of this metabolite on VIC phenotype. These findings suggest that TMAO contributes to the early stages of valve disease by promoting VIC activation and extracellular matrix production through endoplasmic reticulum stress mechanisms. Understanding the role of TMAO and other gut-derived metabolites in the pathogenesis of valve disease could inform the development of novel preventive or therapeutic strategies to modify or delay disease progression. Furthermore, these insights underscore the importance of host-microbiome interactions for cardiovascular health and highlight the potential for targeted dietary interventions to mitigate disease risk.
    Keywords:  Aortic valve disease; ER stress; Gut microbiome; Matrix biology; Metabolites; TMAO; Valvular interstitial cells
    DOI:  https://doi.org/10.1038/s41598-025-32038-2
  22. Pharm Biol. 2026 Dec;64(1): 46-66
       CONTEXT: Chronic heart failure (CHF) is the common concern following myocardial infarction. Xijiaqi Formula (XJQ) effectively treats CHF clinically while the underlying mechanism remains unclarified.
    OBJECTIVE: This study was designed to investigate the effect and mechanism of XJQ on CHF in rats following MI.
    MATERIALS AND METHODS: UHPLC-Q-TOF-MS/MS was utilized to analyze the constituents of XJQ. Post-MI CHF was induced in rats by permanent ligation of the left anterior descending coronary artery. Cardiac function was assessed by echocardiogram and hemodynamic. Myocardial morphology, fibrosis, and ultrastructure were evaluated through HE staining, Masson staining, and transmission electron microscopy, respectively. Myocardial transcriptomics were employed to identify genes that may be altered in response to XJQ treatment. Consistently, XJQ inhibited TGF-β1-induced myofibroblast activation in vitro.
    RESULTS: XJQ significantly improved cardiac function and structure, mitigating fibrosis, edema, and mitochondrial damage, while reducing key biomarkers (BNP, NT-proBNP, cTnT, Ang II). Transcriptomic analysis indicated that the differentially expressed genes influenced by XJQ were predominantly associated with extracellular matrix (ECM) remodeling. Notably, XJQ inhibited the upregulation of ECM proteins, including Adamts2, Fbln1, Itgbl1, and Ltbp3 mRNAs, as well as the proteins TGF-β1, P-Smad2/3, and MMP2. Additionally, in vitro experiments revealed that XJQ significantly suppressed the activation of myofibroblasts induced by TGF-β1.
    CONCLUSIONS: XJQ significantly attenuated the progression from MI to CHF by inhibiting fibroblast activation mediated by TGF-β1/Smads signaling. The molecular mechanisms underlying this effect appear to be intricately linked to its regulation of ECM remodeling proteins, specifically Adamts2, Itgbl1, Fbln1, and Ltbp3.
    Keywords:  TGF-β1; Xijiaqi Formula; chronic heart failure; extracellular matrix remodeling; myocardial fibrosis
    DOI:  https://doi.org/10.1080/13880209.2025.2602234
  23. Nat Commun. 2025 Dec 21.
      Kidney fibrosis is a key pathological feature of chronic kidney disease (CKD), characterized by the activation and accumulation of αSMA-positive myofibroblasts. The cellular origin of myofibroblasts in kidney fibrosis has been a subject of extensive research and debate. Previous studies suggested that myofibroblasts might arise from various cellular sources through mesenchymal transition processes, including epithelial-mesenchymal transition (EMT) of tubular epithelial cells (TECs), endothelial-mesenchymal transition (EndoMT), and macrophage-mesenchymal transition (MMT) of bone marrow-derived cells. In this study, we systematically investigated the origin of myofibroblasts using renal cell lineage tracing tools during kidney fibrosis. Our findings indicated the absence of EMT, EndoMT, and MMT contributing to myofibroblasts, whereas resident fibroblasts were the primary source. Next, we developed and employed specialized dual recombinase-mediated lineage tracing tools, including EMTracer, EndoMTracer, and MMTracer, which revealed reversible partial mesenchymal transition occurring predominantly in the renal urothelial cells (UroCs) and parietal epithelial cells (PECs), minimally in endothelial cells, and not in TECs or macrophages. Our work elucidated the contribution of both complete and partial mesenchymal transition in various renal cell lineages and revealed the origin of myofibroblasts during kidney fibrosis, which may provide important insights into the diagnosis and treatment of CKD.
    DOI:  https://doi.org/10.1038/s41467-025-67373-5
  24. bioRxiv. 2025 Dec 12. pii: 2025.12.10.693501. [Epub ahead of print]
      Rheumatoid arthritis (RA) is a chronic inflammatory disease where the synovial lining membrane undergoes pathological changes resulting in joint destruction. In healthy joints, the synovial lining is essential for joint homeostasis, forming a selective barrier and secreting lubricating molecules, yet the mechanisms that restores homeostatic synovial lining during RA remission remains poorly understood. Here, we applied spatial transcriptomics to examine biopsies of RA patients in remission to identify a mechanism that orchestrates a phenotypic switch specifying synovial quiescent lining fibroblast differentiation. Spatial transcriptomics revealed a proximity-sensing program where at low cell-density, fibroblasts adopt proliferative and fibrotic transcriptional state characterized by expression of MKI67 , COL1A2 and COL6A2 , whereas at high cell-density, fibroblasts induce a quiescent lining fibroblast transcriptional program characterized by PRG4 , CLU and PDPN . Mechanistically, fibroblasts sense spatial proximity through HB-EGF-EGFR signaling, which leads to phosphorylation of transcription factor CREB5. Perturbation of the EGFR-CREB5 axis abolishes fibroblast proximity-sensing and blocks synovial lining fibroblast differentiation. Conversely, EGFR activation by the ligand HB-EGF or pharmacologic activation of CREB5 is sufficient to induce synovial lining fibroblast differentiation. Together, our findings define a novel spatial proximity-sensing pathway underlying a return to homoeostatic fibroblast function during RA remission. By sensing their spatial proximity to neighboring fibroblasts, synovial fibroblasts translate these positional cues into signals that lead to restoration of normal, steady-state synovial lining membrane.
    DOI:  https://doi.org/10.64898/2025.12.10.693501
  25. bioRxiv. 2025 Dec 18. pii: 2025.12.17.693209. [Epub ahead of print]
      The tendon-bone enthesis is a specialized fibrocartilaginous tissue crucial for muscle-to-bone force transmission, yet its postnatal development is not fully understood. Emerging evidence suggests hypoxia plays a pivotal role in enthesis maturation akin to its function in skeletal growth plates, with Hypoxia Inducible Factor 1 alpha (HIF-1α) acting as a key regulator of cellular adaptation (e.g., cell survival, extracellular matrix (ECM) deposition). Here, we investigated the spatial and temporal dynamics of hypoxia in the murine Achilles tendon enthesis and elucidated the role of Hif1a in enthesis cell survival and ECM formation using Scleraxis-lineage conditional knockout (ScxCre; Hif1a cKO) mice. We found that while neonatal tendons rapidly resolve hypoxia after birth, the enthesis maintains a hypoxic niche through postnatal day 5, mirroring a gradient observed in growth plates. Disruption of HIF-1α in enthesis-resident cells resulted in pronounced deficits in grip strength, abnormal tendon-bone attachment morphology, disrupted calcaneal architecture, impaired mineralization, and significant ECM disorganization. Histological analyses revealed persistent cell death and loss of the characteristic fibrocartilaginous gradient in cKO entheses, including dysregulated collagen alignment. In vitro, HIF-1α-deficient tendon fibroblasts exhibited blunted transcriptional responses to hypoxia, altered metabolic gene expression, and changes in ECM deposition. Collectively, our findings illuminate hypoxia as a sustained niche in the postnatal enthesis, with HIF-1α critically required for cell survival, ECM organization, and enthesis structural integrity. This work advances our understanding of enthesis biology and provides insights relevant to tendon-bone attachment disorders and regenerative strategies.
    DOI:  https://doi.org/10.64898/2025.12.17.693209
  26. Exp Eye Res. 2025 Dec 18. pii: S0014-4835(25)00589-5. [Epub ahead of print]264 110816
      Following injury or surgery, quiescent stromal keratocytes can transition into fibroblasts or myofibroblasts leading to either transient or protracted corneal haze. In this study, we investigate the transcriptional changes associated with non-fibrotic wound healing using a transcorneal freeze injury (FI) in the rabbit, which induces full-thickness stromal cell loss without inducing keratocyte-myofibroblast transformation. In control corneas, scRNA-seq revealed multiple clusters expressing markers associated with keratocyte identity (e.g. KERA, LUM, DCN, and ALDH1A1), suggesting heterogeneity in stromal keratocytes in the uninjured stroma. On day 7 after FI, in vivo imaging revealed elongated cells with increased backscatter, consistent with fibroblast migration into the wounded region. Using scRNA-seq, two additional clusters expressing fibroblast markers were also identified. These clusters retained many markers consistent with keratocyte identity, and trajectory analysis demonstrated a continuous progression from quiescent keratocytes to fibroblasts. Both fibroblast clusters had elevated expression genes encoding tenascin C (TNC), claudin 5 (CLDN5), developmental proteoglycans (e.g., BGN, ASPN, VCAN), and cytoskeletal genes (MYL9, MYH10, CDH11), but did not express markers of myofibroblast transformation. Together these genes suggest a mechanically active but non-fibrotic phenotype. One of the two fibroblast clusters also expressed genes related to cell proliferation. By day 28, fibroblastic gene expression was reduced, consistent with resolution of wound healing. These findings define the transcriptional dynamics of intrastromal cell migration following FI and reveal a transient fibroblastic state that supports wound repopulation without fibrosis. Understanding this non-fibrotic repair mechanism could inform strategies to prevent scarring following corneal surgery or injury.
    Keywords:  Confocal microscopy; Corneal stromal fibroblast; Corneal stromal keratocyte; Corneal wound healing; Fibrosis; Single cell RNA-Sequencing; Stromal repopulation
    DOI:  https://doi.org/10.1016/j.exer.2025.110816
  27. Bioorg Chem. 2025 Dec 22. pii: S0045-2068(25)01304-5. [Epub ahead of print]169 109424
      Chronic kidney disease (CKD), characterized by fibrosis, is primarily treated clinically by regulating excessive renin-angiotensin-aldosterone system (RAAS). Our previous research showed that dimeric phthalides from Angelica sinensis had the potential to alleviate CKD by suppressing renin expression and RAAS activation. To advance the search for anti-fibrotic and nephroprotective natural phthalides, a systematic investigation of phthalide polymers of A. sinensis was conducted. In this work, twenty-five dimeric phthalides, including seven new dimers, angesinenolides G-M (1, 13, 17, 18, 22-24), and eighteen known congeners were isolated from A. sinensis. The structures of new compounds were elucidated by spectroscopic and crystallographic data analyses. The anti-fibrosis activities of these phthalides were evaluated in TGF-β1-stimulated HK-2 cells. The results revealed that phthalide dimers 5 (tokinolide A, TA) and 13 significantly reduced the level of renin gene and down-regulated the fibrosis-related protein markers such as fibronectin (Fn), collagen I (Col I), E-cadherin and α-SMA. Mechanistically, treatment with phthalide dimers reduced the levels of renin and Ang II in the RAAS pathway and inhibited the activation of TGF-β1/Smad signaling pathway in TGF-β1-stimulated cells. In the 5/6 nephrectomy (Nx) model, the anti-renal fibrotic efficacy of TA was further substantiated, with in vivo mechanisms consistent with the cellular findings. Overall, these findings expanded the natural phthalide dimers of A. sinensis and supported TA as an attractive lead compound for renal fibrosis and renin-targeted CKD therapy.
    Keywords:  Angelica sinensis; Anti-fibrosis activity; Dimeric phthalides; RAAS; TGF-β1/Smad
    DOI:  https://doi.org/10.1016/j.bioorg.2025.109424
  28. Ann Anat. 2025 Dec 24. pii: S0940-9602(25)00402-9. [Epub ahead of print] 152775
      Musculoskeletal tissue interfaces (TIs), including osteotendinous, myotendinous, and osteochondral junctions, are specialized regions that enable effective force transmission, mechanical stability, and long-term tissue integration. These interfaces are defined by gradients in cellular composition, extracellular matrix (ECM) organization, and mechanical properties, and their maintenance relies in part on tightly regulated cell-matrix interactions. Beyond structural ECM components, matricellular proteins such as Secreted Protein Acidic and Rich in Cysteine (SPARC), thrombospondins, osteopontin, periostin, and tenascins have emerged as critical modulators of interface biology by shaping ECM assembly, mechanotransduction, and adaptive cellular responses to load. SPARC has been shown to impact on collagen fibrillogenesis, ECM organization, and cell-matrix signaling across multiple musculoskeletal tissues. It is increasingly recognized as a regulator of load-bearing musculoskeletal tissue interfaces, where its dysregulation drives maladaptive remodeling marked by fibrosis, ectopic mineralization, and reduced regenerative capacity across pathologies such as tendinopathy, intervertebral disc disease, and osteoarthritis. This mini-review summarizes current knowledge on matricellular regulation at musculoskeletal tissue interfaces, with a focus on SPARC, integrating evidence from genetic models to investigate its role in interface homeostasis, mechanical adaptation, and pathological remodeling.
    Keywords:  IVD interface; SPARC; enthesis; myotendinous junction; osteochondral junction; tissue interface
    DOI:  https://doi.org/10.1016/j.aanat.2025.152775
  29. Phytomedicine. 2025 Nov 29. pii: S0944-7113(25)01232-2. [Epub ahead of print]150 157597
       BACKGROUND: Psoriasis is a chronic inflammatory skin disease often referred to as the "incurable cancer," characterized by a long disease course, high recurrence rate, and inability to achieve complete cure. It not only severely impacts patients' quality of life but also faces challenges such as high treatment costs and side effects with current therapeutic approaches. The primary active component of pine pollen (PP) extract (PPE) is dihydroquercetin (DHQ), which possesses various pharmacological activities, including anti-inflammatory, antioxidant, and immune-modulating effects. To date, however, the pharmacological properties and mechanism of action of DHQ remain uncharacterised, and further evidence is required to substantiate its efficacy in treating psoriasis.
    OBJECTIVE: This study sought to examine the anti-psoriatic properties of PPE, determine its principal active component, and clarify its mechanisms of action along with its therapeutic prospects.
    METHOD: This study elucidated the anti-psoriatic mechanism of PPE. Bioactivity-directed purification afforded a PPE enriched with DHQ. Subsequent phytochemical analysis employing UPLC-Q-Orbitrap/MS and HPLC identified DHQ and 17 additional active constituents. The mechanism of action was predicted through an integration of network pharmacology and molecular docking, with predictions subsequently validated by RT-qPCR. In LPS-induced RAW 264.7 macrophages, a 24-hour intervention with PPE modulated levels of ROS, apoptosis, mitochondrial membrane potential, cell migration, and inflammatory responses. In a 5 % IMQ-induced murine psoriasis model, seven-day oral administration of PPE conferred therapeutic efficacy, as assessed by PASI scoring, histological and immunohistochemical examination, ELISA, and Western blot analysis.
    RESULTS: PPE treatment significantly reduced PASI scores, skin thickness, splenic index, and inflammatory cell infiltration. It also reversed intestinal barrier damage, ameliorated small intestinal villus atrophy, and suppressed serum levels of inflammatory cytokines. PPE alleviated psoriasis by inhibiting macrophage-driven inflammation. Integrated UPLC-Q-Orbitrap/MS and HPLC analyses, combined with network pharmacology and molecular docking, identified DHQ as the primary active constituent of PPE. Consistent with Western blot and immunohistochemical findings, molecular analyses confirmed that PPE ameliorated IMQ-induced psoriasiform dermatitis and modulated Th17-related gene expression-including IL-17, IL-6, IL-1β, TNF-α, IFN-γ, and keratins. These results suggest that PPE exerts its therapeutic effect by modulating the IL-17 signalling pathway, mediated by HO-1/Nrf2, NF-κB, and JAK1/STAT3, which may represent critical targets in PPE-mediated treatment.
    CONCLUSION: This study presents the first comprehensive investigation into the anti-psoriatic effects of PPE, wherein the complex mechanisms underlying its therapeutic action are elucidated. It is demonstrated that psoriatic inflammation and oxidative stress are alleviated by PPE, while immune function is modulated through regulation of the IL-23/Th17 axis and the Nrf2/HO-1, NF-κB, and JAK1/STAT3 signalling pathways. By extending beyond the specific compound and disease model under investigation, novel insights are provided that support the establishment of a new research paradigm for developing more effective clinical therapies.
    Keywords:  Dihydroquercetin; Immunological; Macrophage; Pinaceae; Pine pollen; Pinus massoniana Lamb.; Psoriasis
    DOI:  https://doi.org/10.1016/j.phymed.2025.157597