bims-cesemi Biomed News
on Cellular senescence and mitochondria
Issue of 2026–03–01
nine papers selected by
Julio Cesar Cardenas, Universidad Mayor



  1. Cancers (Basel). 2026 Feb 08. pii: 550. [Epub ahead of print]18(4):
      Cellular senescence has been traditionally viewed as a tumor-suppressive program that halts its proliferation in response to oncogenic stress or DNA damage. However, recent studies have highlighted a paradoxical role for senescence in glioblastoma (GBM), IDH-wildtype, the most aggressive primary brain tumor in adults. Accumulating evidence indicates that senescence represents a "frequent and durable" cell fate in GBM, particularly following standard therapies such as temozolomide and radiotherapy. Senescent cells frequently persist after temozolomide or radiotherapy and acquire a senescence-associated secretory phenotype (SASP) composed of inflammatory cytokines, growth factors and matrix-remodeling enzymes. These factors not only promote tumor cell survival with stemness-induction but also reshape the pro-tumorigenic microenvironment with metabolic rewiring and immune evasion. Notably, senescence also arises in non-malignant cells-including astrocytes, endothelial cells, microglia, and infiltrating immune cells-creating a multicellular senescent niche that fuels recurrence. Here, we describe a recent advance in our understanding of senescence and SASP in the pathobiology of GBM. We further focus on a state-of-the-art, challenging exploration of the idea that single-cell and spatial profiling, capable of identifying senescence- and SASP-associated morphologic and heterogeneous states, will further refine patient selection and therapeutic timing. By reframing senescence as a modifiable determinant of GBM evolution, this review underscores its emerging significance as both a cancer hallmark and a therapeutic vulnerability.
    Keywords:  SASP; glioblastoma; glioma stem-like cells; inflammatory–metabolic coupling; senolytics; senomorphics; therapy-induced senescence
    DOI:  https://doi.org/10.3390/cancers18040550
  2. Nat Commun. 2026 Feb 25. pii: 1656. [Epub ahead of print]17(1):
      VO2peak is a key health benefit of aerobic exercise; however, chronic hyperglycemia is associated with persistently low VO2peak due to an impaired adaptive response to training. Here, we show that reducing blood glucose with a carbohydrate-restricted, high fat ketogenic diet can restore aerobic exercise adaptation in male mice with hyperglycemia. Hyperglycemic mice received standard high-carbohydrate chow (CHOW), which sustains high blood glucose; or a ketogenic diet (KETO), which normalizes blood glucose levels. After aerobic exercise training, improvements in VO2peak are blunted in CHOW, but restored by KETO. Increased VO2peak in KETO is associated with enhanced aerobic remodeling of skeletal muscle, including a more oxidative fiber-type and increased capillary density. Moreover, KETO induces exercise-independent effects on muscle mitochondrial remodeling and substrate selection, significantly increasing fatty acid oxidation and down-regulating glucose metabolism. We identify a ketogenic diet as a potential therapy to improve aerobic exercise adaptation in the growing population with hyperglycemia.
    DOI:  https://doi.org/10.1038/s41467-026-69349-5
  3. Neuro Oncol. 2026 Feb 23. pii: noag038. [Epub ahead of print]
      Glioblastoma (GBM) is a highly aggressive and metabolically adaptable brain tumor characterized by profound cellular heterogeneity and therapy resistance. Recent research has uncovered the phenomenon of horizontal mitochondrial transfer (HMT) between GBM cells and their microenvironment, particularly astrocytes, which contributes to tumor progression, metabolic reprogramming, and treatment resistance. This review summarises current knowledge on mitochondrial exchange in GBM via tunneling nanotubes (TNTs), tumor microtubes (TMs) and potentially via extracellular vesicles (EVs). It also explores the functional consequences of HMT, including enhanced oxidative phosphorylation (OXPHOS), increased tumorigenicity, and altered therapeutic responses. This review highlights the need for further investigation into the molecular drivers and context-specific outcomes of mitochondrial transfer in GBM, with implications for novel therapeutic strategies.
    Keywords:  Glioblastoma; OXPHOS; mitochondria transfer; tumor microtubes; tunneling nanotubes
    DOI:  https://doi.org/10.1093/neuonc/noag038
  4. J Dent Res. 2026 Feb 24. 220345251411909
      Saliva secretion requires continuous energy supply throughout the day. Mitochondria dynamically adapt to fluctuating energy demands, yet the mechanisms underlying the adaptions remain poorly understood. Here, we employed real-time intravital imaging and fluorescence lifetime imaging microscopy (FLIM) to monitor mitochondria functions in submandibular glands. We revealed distinct mitochondrial distribution patterns; in acinar cells, mitochondria were predominantly distributed near the cell membranes or scattered throughout the cytoplasm with extensive endoplasmic reticulum (ER)-mitochondria contact sites, whereas in ductal cells, mitochondria were densely packed within the cytoplasm. At resting states, mitochondria exhibited larger volumes, fewer numbers, and higher oxidative phosphorylation activity in acinar cells compared with those in ductal cells. Upon stimulation with pilocarpine, mitochondrial motility, NAD(P)H levels, NAD(P)H enzyme-bound fractions, and mitochondrial adenosine triphosphate (ATP) production were significantly elevated. Pilocarpine-induced secretion, mediated by both aquaporin 5 translocation and the opening of paracellular pathway, was markedly attenuated by oligomycin A, an ATP synthase inhibitor. Notably, pilocarpine increased mitochondria-ER contact sites to 1.7 times the control level (from 18% to 31%), and blocking mitochondrial calcium uptake significantly suppressed pilocarpine-induced NAD(P)H and ATP production. These findings highlight the critical role of ER-mitochondria calcium transfer in sustaining bioenergetics required for salivary secretion, providing new insights into mitochondrial functional adaptation and its physiological significance in intact secretory systems.
    Keywords:  NADH; energy metabolism; mitochondria associated membranes; muscarinic acetylcholine receptor; secretion; submandibular gland
    DOI:  https://doi.org/10.1177/00220345251411909
  5. bioRxiv. 2026 Feb 09. pii: 2026.02.05.704021. [Epub ahead of print]
      Glioblastoma (GBM) stem-like cells (GSCs) contribute to therapeutic resistance and recurrence. We sought to define cellular processes underlying GSC resilience. We discovered that GSCs, unlike differentiated GBM cells (DGCs) or non-malignant neural cells, depend on mitochondrial function for survival. To target this vulnerability, we exploited doxycycline (DOXY), an antibiotic used in humans, to interfere with mitochondrial protein translation. DOXY induced cell death and inhibited sphere formation in GSCs, but not in DGCs or non-malignant cells, indicating a differentiation state-selective effect. Mechanistically, DOXY induced mitochondrial dysfunction and activated a stress-responsive apoptotic program involving HRI-mediated signaling. DOXY displayed antitumor efficacy in patient-derived GBM organoid and orthotopic xenograft models. Our study reveals that DOXY can selectively target undifferentiated glioma cells, informing a drug repurposing-based strategy.
    DOI:  https://doi.org/10.64898/2026.02.05.704021
  6. Free Radic Biol Med. 2026 Feb 19. pii: S0891-5849(26)00147-4. [Epub ahead of print]248 210-221
      Alpha-ketoglutarate dehydrogenase (KGDH; EC 1.2.4.2) catalyzes the fourth step of the tricarboxylic acid (TCA) cycle and links carbohydrate, fatty acid and amino acid metabolism to the aerobic production of ATP. KGDH is classically viewed as indispensable to energy metabolism and strictly located to mitochondria. Therefore, it is generally thought that the loss of its activity has catastrophic consequences for mammalian cells. However, recent advances in molecular biology and redox biology tools coupled with the implementation of new genetically modified mouse lines and cultured cells knocked down for components of KGDH have revealed it is a multifunctional cellular enzyme that localizes to the mitochondria and nucleus where it uses superoxide (O2•-)/hydrogen peroxide (H2O2) and metabolites related to its catalysis (e.g., alpha-ketoglutarate (KG), succinyl-CoA, succinate) to control cell fate decisions. In addition, it has been revealed that over-stimulation of KGDH causes severe oxidative stress through the hyper-production of O2•-/H2O2 and disturbs cell signals and epigenome regulation, which has been linked to cancer cell transformation, metabolic diseases like metabolic dysfunction-associated steatotic liver disease (MASLD), and inflammation. Furthermore, inhibition of KGDH with competitive inhibitors, redox modifications, or shRNAs has shown that the targeted disruption of the enzyme can alleviate these diseases. The aim of this review is to update the literature on KGDH. It is not just a TCA cycle enzyme anymore.
    DOI:  https://doi.org/10.1016/j.freeradbiomed.2026.02.050
  7. Trends Mol Med. 2026 Feb 26. pii: S1471-4914(25)00289-8. [Epub ahead of print]
      In recent years, numerous studies have highlighted the crucial role of mitochondrial metabolism in cancer progression. This sparked interest in its potential as a target for cancer therapy and prompted the clinical evaluation of multiple drugs targeting mitochondrial metabolism. Regrettably, most have showed limited efficacy and safety, raising concerns about the viability of mitochondrial inhibitors in cancer treatment. However, emerging evidence suggests that shifting the focus away from mitochondrial bioenergetics and targeting other aspects of mitochondrial biology, may have a meaningful impact on cancer progression with milder side effects. In this review, we discuss emerging actionable targets and strategies to tailor the administration of inhibitors of mitochondrial pathways for cancer therapy.
    Keywords:  cancer; metabolism; metastasis; mitochondria; mitochondrial dynamics
    DOI:  https://doi.org/10.1016/j.molmed.2025.12.002
  8. Adv Wound Care (New Rochelle). 2026 Feb 23. 21621918261426580
       OBJECTIVE: Diabetes mellitus affects over 25% of adults aged 65+ in the United States and is associated with a heightened risk of developing diabetic foot ulcers. Accumulation of senescent cells within the wound microenvironment can impair cutaneous repair, and senolytic therapies offer a promising approach to accelerate wound healing.
    APPROACH: In this study, topical fisetin, a flavonoid that promotes apoptosis of senescent cells, was evaluated for its impact on diabetic wound repair. Full-thickness excisional wounds were created on the dorsal skin of diabetic (db/db) mice. Animals were randomized to receive either topical vehicle (n = 12) or fisetin (n = 12) for three consecutive days per week, and wound healing outcomes were longitudinally assessed.
    RESULTS: Topical fisetin significantly increased the ratio of healthy dermis to granulation by day 7 (p = 0.04) and reduced dermal fibrosis by day 21 (p = 0.03). Fisetin decreased p16+ cells (p = 0.01) but increased p21+ cells (p = 0.02) at day 7 in the dermis, indicating varied effects on senescent cells. M1 macrophages (CD80+) were decreased in the fisetin-treated group (p = 0.05) at day 21, accompanied by a decrease in pro-inflammatory senescence-associated secretory phenotype cytokines, tumor necrosis factor alpha (p = 0.03), and interleukin-1beta (p = 0.01) at day 7.
    INNOVATION: Fisetin is the first topical seno-modulatory agent shown to enhance wound repair when administered after injury onset. Its favorable safety and efficacy in both modulating senescence and inflammation highlight its potential as a novel therapy for diabetic wounds.
    CONCLUSION: Topical fisetin enhances diabetic wound healing by reducing fibrosis and promoting healthy dermal regeneration through senescence and inflammation modulation. [Figure: see text].
    Keywords:  diabetes; fibrosis; fisetin; granulation; macrophages; wounds
    DOI:  https://doi.org/10.1177/21621918261426580
  9. medRxiv. 2026 Feb 09. pii: 2026.02.06.26345739. [Epub ahead of print]
      Cellular senescence increases in frequency with age and is implicated in age-related pathologies, and identifying circulating biomarkers of senescence holds great diagnostic potential. Circulating senescence signatures are predictive of many age-related traits and diseases, though cell type-specific senescence signatures have not been comprehensively explored. In this study, senescence signatures from the Senescence Catalog (SenCat), including 14 human cell types such as peripheral blood mononuclear cells, renal epithelial cells, vascular smooth muscle cells, among others, are examined for their clinical relevance in circulation in two longitudinal studies: 1,275 participants of the Baltimore Longitudinal Study of Aging (BLSA) and 997 participants of the Invecchiare in Chianti (InCHIANTI) study. Notably, pooled senescence proteins outperformed non-senescence proteins in predicting many clinical parameters such as age and hypertension, and in many instances cell type senescence signatures mapped most strongly to their corresponding health domain. Importantly, the immune cell senescence signature is associated with future onset of several diseases such as diabetes. This study demonstrates that circulating cell type-specific biomarkers of senescence can reveal higher resolution health status than previously attained.
    HIGHLIGHTS: Circulating senescence associated proteins tend to outperform non-senescence proteins as biomarkers of clinical phenotypes in two independent longitudinal studies.A core senescence signature developed from 14 human cell types predicted a range of clinical phenotypes during aging.Cell type senescence signatures more strongly associated with their corresponding health domains.The immune cell senescence signature and others were associated with mortality and diabetes onset, highlighting relevance for assessing health trajectories.
    DOI:  https://doi.org/10.64898/2026.02.06.26345739