bims-engexo Biomed News
on Engineered exosomes
Issue of 2025–10–19
eleven papers selected by
Ravindran Jaganathan, Universiti Kuala Lumpur



  1. Tissue Cell. 2025 Oct 09. pii: S0040-8166(25)00460-4. [Epub ahead of print]98 103178
      Wound healing, particularly in chronic wounds, remains a significant clinical challenge due to delayed recovery and limited efficacy of conventional treatments. Exosomes, which are nanosized extracellular vesicles released by cells, are promising mediators of intercellular communication and repair processes. They regulate angiogenesis, collagen synthesis, inflammation, and scar formation, thereby accelerating tissue repair. Recent evidence highlights that stem cell-derived exosomes can serve as a cell-free therapeutic alternative with superior efficacy and lower tumorigenic risk compared to stem cell transplantation because of their regenerative secretome. This review critically summarizes the current applications of exosomes in wound healing, including their role as natural drug carriers, interactions with biomaterials for sustained release, and modulation of molecular pathways across different healing phases. Furthermore, we discuss advances in engineered exosomes, recent clinical and preclinical results, and persisting challenges such as standardization, large-scale production, and safety considerations. By consolidating existing knowledge and future directions, this study underscores the potential of exosomes as a next-generation therapeutic platform to improve wound repair.
    Keywords:  Wound healing; exosomes; extracellular vesicle; mechanism therapeutics; mesenchymal stem cells
    DOI:  https://doi.org/10.1016/j.tice.2025.103178
  2. Vet Microbiol. 2025 Oct 13. pii: S0378-1135(25)00398-0. [Epub ahead of print]311 110762
      Circular RNAs (circRNAs) play crucial roles in various physiological and pathological processes, including the complex interactions between viruses and hosts. However, the regulatory mechanism by which porcine milk exosome-derived circRNAs affect porcine epidemic diarrhea virus (PEDV) replication remains poorly understood. Building on our previous sequencing analysis of non-coding RNAs in porcine milk exosomes, we identified circRNA molecules that may regulate PEDV replication in the intestines of piglets and validated these findings at both the cellular and piglet intestinal organoid levels. The results demonstrated that circLSM14A was present in porcine milk exosomes, acted as an endogenous miR-27b-5p sponge, and sequestered and inhibited miR-27b-5p activity. This inhibition increased the expression of high mobility group protein 1 (HMGB1), which subsequently promoted the expression of downstream signaling molecules, including TLR4, NF-κB1, NF-κB2, Rel, and Beclin1, and ultimately enhanced PEDV replication at cellular and intestinal organoid levels. This study identifies circLSM14A as one of the regulators involved in PEDV replication in porcine milk exosomes. These findings advance our understanding of the biological functions of circLSM14A and clarify the role of non-coding RNAs carried by milk exosomes in regulating PEDV replication. This research provides new insights and approaches for the prevention and control of PEDV.
    Keywords:  CircLSM14A; HMGB1; PEDV; Viral replication; miR-27b-5p
    DOI:  https://doi.org/10.1016/j.vetmic.2025.110762
  3. Front Immunol. 2025 ;16 1667122
      Epilepsy, as a chronic neurological disorder marked by recurrent seizures, is closely linked to neuroinflammation and immune dysregulation. Exosomes, extracellular vesicles with potent immunomodulatory properties, have emerged as key players in mitigating epilepsy-associated inflammation by targeting glial activation and balancing pro- and anti-inflammatory cytokine release. Their ability to cross the blood-brain barrier (BBB) enables targeted delivery of anti-inflammatory cargo, such as miRNAs and proteins, offering promise for diagnosing and treating drug-resistant epilepsy. This review highlights exosomes' dual role as biomarkers of inflammatory pathways and therapeutic vehicles for immune modulation. By suppressing neuroinflammation and restoring neuronal homeostasis, exosome-based strategies may revolutionize epilepsy management, though clinical translation requires further optimization of isolation and engineering techniques.
    Keywords:  blood-brain barrier; drug delivery; drug-resistance; epilepsy; exosomes; neuroinflammation
    DOI:  https://doi.org/10.3389/fimmu.2025.1667122
  4. FASEB J. 2025 Oct 31. 39(20): e71110
      Bone marrow mesenchymal stem cells (BMSCs) can differentiate into osteoblasts and promote osteogenesis (OP), and the miRNAs carried by BMSCs-derived exosomes (BMSC-Exo) regulate osteoblast differentiation in bone-related diseases. Additionally, abnormal mitochondrial autophagy in osteoblasts mediated by the SIRT1/PINK1/Parkin signaling axis affects differentiation and contributes to OP progression. Our preliminary study has demonstrated that miR-20b can target SIRT1 and osteogenic protein BMP2. The aim of the present study was to investigate the effect of BMSC-Exo harboring miR-20b to mediate the SIRT1/BMP2 in OP. Initially, through the successful isolation and characterization of BMSC-Exo in vitro, we co-cultured these exosomes with osteoblasts and observed a significant enhancement in osteoblast differentiation, alkaline phosphatase activity, and mineral accumulation. Subsequent cell transfection experiments revealed that miR-20b-overexpressed BMSC-Exo further augmented osteogenic differentiation of osteoblasts, whereas interference with BMP2 expression attenuated this pro-osteogenic effect. In a bilateral ovariectomised rat model of OP, we demonstrated that miR-20b-overexpressed BMSC-Exo treatment promoted bone formation and mitigated bone damage. Additionally, these exosomes restored mitochondrial membrane potential and autophagy, which were reversed by SIRT1 interference. Finally, osteoblasts isolated from OP model rats were used to further validate that miR-20b-overexpressed BMSC-Exo enhanced osteoblast differentiation and facilitated osteogenesis by activating SIRT1. These findings have collectively underscored the therapeutic potential of miR-20b-enriched BMSC-Exo in regard to OP treatment, providing a foundation for developing novel, targeted therapies for OP.
    Keywords:  SIRT1/BMP2; bone marrow mesenchymal stem cell; exosomes; miR‐20b; mitochondrial autophagy; osteoblast; osteoporosis
    DOI:  https://doi.org/10.1096/fj.202501050RR
  5. Front Cell Dev Biol. 2025 ;13 1605174
      Female infertility and reproductive disorders represent a significant global health challenge, with complex etiologies often linked to impaired cellular communication, inflammation, and tissue dysfunction. Exosomes (EXOs), nanosized extracellular vesicles laden with bioactive molecules, have become recognized as significant transmitters of intercellular signaling in reproductive physiology and pathology. This review comprehensively discusses the dual diagnostic and therapeutic potential of EXOs in addressing female infertility disorders, such as endometriosis, polycystic ovary syndrome (PCOS), primary ovarian insufficiency (POI), Asherman syndrome, and gynecological cancers. We investigate the strategies whereby EXOs govern important activities like endometrial regeneration, folliculogenesis, immune modulation, and angiogenesis, while highlighting their role in restoring ovarian and uterine homeostasis. Advances in exosome isolation techniques, bioengineering strategies (e.g., cargo loading, surface modification), and scaffold-based delivery systems are critically evaluated for their capacity to enhance therapeutic precision and efficacy. Notwithstanding their potential, issues include standardization of isolation protocols, scalability, and long-term safety, which necessitate further research. By integrating molecular insights with translational innovations, this review underscores the clinical implementation of exosome-based therapeutics in revolutionizing reproductive medicine, offering new hope for personalized, non-invasive treatments in female fertility restoration.
    Keywords:  extracellular vesicles; gynecological cancers; nanomedicine; regenerative medicine; stem cell; tissue engineering
    DOI:  https://doi.org/10.3389/fcell.2025.1605174
  6. Transl Oncol. 2025 Oct 16. pii: S1936-5233(25)00295-5. [Epub ahead of print]62 102564
       OBJECTIVE: To explore the effect of exosome-mediated miR-199b-5p on lung cancer cells behavior, intrapulmonary metastasis, and its underlying mechanism.
    METHODS: Exosomes from SK-LU-1 cells overexpressing has-miR-199b-5p (miR-199b-5p) were used to treat A549 or H299 cells. Cell motility was evaluated using wound scratch healing and transwell assays. Gene and protein expression were detected by quantitative real-time PCR (QRT-PCR) and Western blot. Target genes of miR-199b-5p were predicted through multiple-database analysis and validated.
    RESULTS: Transmission electron microscopy (TEM) demonstrated isolated exosomes had a typical bilayer membrane (30-100 nm). miR-199b-5p was highly expressed in lung cancer cells and detectable in the serum of lung cancer patients, with the highest levels observed in SK-LU-1 cells and their derived exosomes. Exosomal miR-199b-5p significantly enhanced the motility of A549 and H1299 cells and upregulated the expression of epithelial-mesenchymal transition (EMT)-related proteins. Exosomes promoted lung metastasis of H1299 cells and inhibited the expression of Cyclin L1 (CCNL1). Either CCNL1 inhibition or miR-199b-5p overexpression significantly promoted H1299 cell proliferation and reduced apoptosis, while CCNL1 overexpression inhibited cell motility. Protein-protein interaction (PPI) network, Gene Ontology (GO), and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses indicated involvement of the Wnt/β-catenin signaling pathway in the downstream mechanism. Mechanistically, miR-199b-5p inhibited cyclin-dependent kinase 11 (CDK11) and upregulated the expression of transcription factor 4 (TCF-4) and β-catenin.
    CONCLUSIONS: Overexpression of miR-199b-5p promotes proliferation, migration, and EMT in lung cancer cells by targeting CCNL1, with its downstream regulatory effects mediated through the Wnt/β-catenin signaling.
    Keywords:  Cell cycle; Epithelial-mesenchymal transition; Exosomes; Wnt/β-catenin
    DOI:  https://doi.org/10.1016/j.tranon.2025.102564
  7. Drug Des Devel Ther. 2025 ;19 9099-9115
       Background: Primary osteoporosis imposes a growing global burden. While antiresorptive and anabolic agents reduce fractures, long-term adherence, adverse events, and limited tissue targeting leave unmet needs. Exosomes have emerged as promising, cell-free candidates.
    Methods: We conducted a narrative synthesis of English-language studies (2010-May 2025) indexed in PubMed and Web of Science on exosomes and primary osteoporosis, including mechanistic, preclinical efficacy, delivery, and safety data.
    Results: Exosomes modulate bone remodeling via osteoanabolic signaling, osteoclast inhibition, and antioxidative pathways. Across cell and animal models, exosome preparations improved osteoblast viability and function, enhanced mineralization, and mitigated glucocorticoid- or estrogen-deficiency-related bone loss. Key translational variables include source selection, isolation/characterization, cargo loading, dosing, route, targeting, and biocompatibility. Safety signals are preliminarily favorable but heterogeneous across platforms. The current evidence base is predominantly preclinical; standardized manufacturing, biodistribution and persistence profiling, and dose-response relationships remain insufficient.
    Conclusion: Exosome-based approaches are promising adjuncts rather than immediate replacements for current osteoporosis therapies. Priorities include harmonized release criteria, head-to-head comparisons with standard agents, validated pharmacodynamic biomarkers, and early-phase clinical trials.
    Clinical Relevance: For patients who are intolerant of or inadequately controlled by approved agents, exosome strategies may offer future targeted adjuncts once quality, safety, and efficacy are established in humans.
    Keywords:  bone regeneration; drug delivery; exosomes; primary osteoporosis; targeted therapy
    DOI:  https://doi.org/10.2147/DDDT.S550797
  8. ACS Appl Bio Mater. 2025 Oct 15.
      A delayed healing process in diabetic wounds is intractable. In this study, a high-glucose condition was found to be responsible for skin structure destruction, inflammatory infiltration, and vital cell dysfunction. Extracellular vesicles, particularly exosomes secreted by hucMSCs, contribute to improved diabetic wound healing, largely by promoting tissue repair and re-establishing normal function in affected cells. Small RNA-sequencing revealed that hucMSC-derived exosomes (hucMSC-Ex) were highly enriched in NC_000019.10_13474 (miR-13474), which was predicted to be an miRNA with an undiscovered function. miR-13474 showed a reduced expression level in high-glucose-treated skin cells as well as diabetic foot ulcer (DFU) rats. Moreover, there is also a significant expression difference between the wound area and the wound edge in DFU patients, indicating the potential clinical value of miR-13474. Blocking miR-13474 in hucMSC-Ex obviously diminished the therapeutic effects. Furthermore, exosomal miR-13474 was found to target the CPEB2/TWIST1 axis to improve the impaired function of skin cells. On this basis, hucMSC-Ex were used as a vehicle for the delivery of therapeutic miR-13474 to optimize the repairing effect. The study has revealed the role of hucMSC-derived exosomes and the underlying molecular mechanism in diabetic wound healing and proposes a cell-free-based modification strategy for refractory wound management.
    Keywords:  diabetic wound healing; exosomes; miRNAs; small extracellular vesicles; therapy
    DOI:  https://doi.org/10.1021/acsabm.5c01352
  9. Neurochem Res. 2025 Oct 14. 50(5): 326
      Neuroinflammation mediated by reactive microglia and astrocytes is the primary pathological process of early brain injury (EBI) after subarachnoid hemorrhage (SAH). This study aimed to investigate the role of microglia-derived exosomes in astrocytic activation and neuronal damage in SAH. An SAH mouse model was generated via endovascular perforation. Following the administration of miR-223-3p-enriched microglia-derived exosomes or a CCL11 antibody (anti-CCL11), the neurological functions of mice were evaluated. Nissl staining and TUNEL staining were carried out to assess neuronal apoptosis. The activation of microglia and astrocytes was examined by immunofluorescence. Hemin-treated primary cultured microglia and astrocytes were then cocultured with miR-223-3p-enriched exosomes or anti-CCL11. Furthermore, the conditioned medium of the cells was collected and added to HT22 cells. The viability, ROS level, and degree of oxidative stress in HT22 cells were determined. The mechanism of miR-223-3p to target RhoB was verified via a dual-luciferase reporter gene assay. Reduced miR-223-3p expression was detected in SAH mice, whereas CCL11 and inflammatory cytokines (IL-1β, IL-6, TNF-α, and IL-18) were elevated. Microglia-derived exosomal miR-223-3p or anti-CCL11 significantly mitigated neurological deficits and neuronal damage, and relieved microglial and astrocytic activation in the SAH model. In vitro experiments revealed that hemin induced significant activation of microglia and astrocytes. MiR-223-3p-enriched exosomes or anti-CCL11 attenuated hemin-induced microglial and astrocytic activation and attenuated HT22 cell damage through the inhibition of ROS and oxidative stress. Mechanistic studies revealed that miR-223-3p targeted RhoB and inhibited the RhoB/NF-κB/CCL11 axis in astrocytes. Microglia-derived exosomal miR-223-3p relieves EBI after SAH through the inhibition of astrocytic activation via the RhoB-NF-κB-CCL11 pathway.
    Keywords:  Astrocyte; Exosome; Microglia; Subarachnoid hemorrhage; miR-223-3p
    DOI:  https://doi.org/10.1007/s11064-025-04566-w
  10. Front Cardiovasc Med. 2025 ;12 1572045
       Background: Vascular calcification (VC) is a critical pathological characteristic of cardiovascular diseases like atherosclerosis, frequently linked to phenotypic alterations in vascular smooth muscle cells (VSMCs) and the activation of bone-forming genes. Exosomes derived from bone marrow mesenchymal stem cells (BMSCs) have been shown to significantly attenuate VSMC calcification.
    Methods: To investigate whether BMSC-derived exosomes mitigate VSMC calcification through microRNAs (miRNAs) regulation, we developed an in vitro model using β-glycerophosphate-induced calcification and an in vivo model using vitamin D3-induced calcification. Exosomes were extracted from BMSC culture media via ultracentrifugation and analyzed using transmission electron microscopy and particle size distribution assays.
    Results: Functional and phenotypic assessments revealed that BMSC-derived exosomes markedly reduced VSMC calcification. RT-qPCR analysis further indicated that BMSC-derived exosomes regulate VSMC calcification by modulating rno-miR-335 (miR-335). The miR-335 mimic notably suppressed the expression of the osteogenic regulator RUNX2 in VSMCs. Dual-luciferase reporter assays demonstrated that SP1 is a direct target of miR-335. Exosomal miR-335 inhibited SP1 expression, resulting in reduced mRNA and protein levels of RUNX2. In vivo studies confirmed that agomiR-335 treatment significantly lowered SP1 levels in the aorta of male SD rats, alleviating vitamin D3-induced VC.
    Conclusion: This study highlights that BMSC-derived exosomes regulate VC via the miR-335/SP1 axis, offering novel molecular targets for treating VC.
    Keywords:  BMSCs; RUNX2; SP1; VSMCs; exosomes; miR-335; vascular calcification
    DOI:  https://doi.org/10.3389/fcvm.2025.1572045
  11. Int J Surg. 2025 Oct 14.
       BACKGROUND: Sepsis induces complex immunological responses; however, the role of circulating exosomes in regulating macrophage function and T cell responses remains unknown. This study examined the effects of sepsis-derived exosomes on macrophages and their subsequent T cell differentiation.
    MATERIALS AND METHODS: A cecal ligation and puncture (CLP) model was used to induce sepsis in C57BL/6 mice. Exosomes were isolated from the blood of septic (CLP-exo) and sham-operated (Control-exo) mice. Their effects on macrophage proliferation, polarization, and phagocytic function were assessed in vitro. T cell responses were evaluated through co-culture experiments with CLP-exo-treated or Control-exo-treated macrophages and in vivo studies.
    RESULTS: CLP-exo inhibited macrophage proliferation, induced apoptosis, and suppressed M2 polarization. Phagocytic function was impaired and accompanied by increased PD-1 expression. Co-culture of T cells with CLP-exo-treated macrophages activated the KLF4 pathway and increased Th17-related cytokine expression. In vivo, PD-1 expression in CLP-exo-treated macrophages was associated with enhanced T cell differentiation toward the Th17 subtype in blood. PCR array analysis revealed the activation of multiple T cell-related genes, including Csf2, IL-2, IL-4, STAT4, and STAT6.
    CONCLUSION: Sepsis-derived exosomes induced PD-1 expression in macrophages and promoted Th17 differentiation, revealing a novel mechanism of immune dysregulation in sepsis. These findings provide new insights into immune dysregulation in sepsis pathophysiology.
    Keywords:  T lymphocytes; exosomes; kruppel-like factor 4 (KLF4); macrophages; programmed cell death 1 (PD-1); sepsis
    DOI:  https://doi.org/10.1097/JS9.0000000000003651