bims-cesemi Biomed News
on Cellular senescence and mitochondria
Issue of 2026–04–19
six papers selected by
Julio Cesar Cardenas, Universidad Mayor



  1. J Physiol. 2026 Apr 14.
      Sprint interval exercise (SIE) induces skeletal muscle mitochondrial adaptations that are comparable to, or greater than, those observed with moderate-intensity continuous exercise (MICE), despite requiring a lower training volume. Previous work has shown that these adaptations are at least partly mediated by enhanced mitochondrial bioenergetics, including increased mitochondrial Ca2+ uptake and resulting pyruvate dehydrogenase (PDH) activation. In parallel, the natural compound oleuropein from olive leaf extract (OLE) promotes mitochondrial Ca2+ uptake and activates PDH in mouse skeletal muscle. Here, we tested the hypothesis that OLE intake would activate PDH and potentiate mitochondrial adaptations in human skeletal muscle during either MICE or SIE. In a crossover, double-blind study, healthy males performed MICE (1 h at 50% maximal aerobic power, n = 11) or SIE (6 × 30 s all-out sprints with 4 min recovery, n = 10). Knee extensor neuromuscular tests and vastus lateralis muscle biopsies were performed before, immediately after and 24 h after SIE or MICE. OLE improved the decline of power output during the first sprint in SIE and reduced heart rate during MICE but did not affect knee extensor fatigability after both exercise modalities. Transcriptomic analyses revealed an effect of OLE on the mitochondrial and inflammatory response after MICE and SIE, while OLE increased PDH activity in combination with exercise only following MICE. Together, these results suggest that OLE modulates skeletal muscle response to exercise and pave the way for future investigations aiming to investigate the chronic effect of combining OLE and exercise training. KEY POINTS: Previous studies have shown that oleuropein increases mitochondrial calcium uptake in preclinical models and that mitochondrial calcium uptake contributes to skeletal muscle mitochondrial adaptations in response to maximal intensity exercise in humans. Olive leaf extract (OLE) increases the activity of pyruvate dehydrogenase, a proxy of mitochondria calcium uptake, when combined with moderate-intensity exercise. Combining moderate-intensity continuous exercise and sprint interval exercise with OLE enhances the mitochondrial response at a transcriptional level. OLE enhances skeletal muscle mitochondrial response to acute exercise, paving the way for investigating its effect in combination with chronic exercise training protocols.
    Keywords:  calcium mitochondria; muscle fatigue; oxidative phosphorylation; power output; pyruvate dehydrogenase
    DOI:  https://doi.org/10.1113/JP290316
  2. Nat Commun. 2026 Apr 14.
      Transmembrane protein 65 (TMEM65) depletion in a patient caused severe mitochondrial encephalomyopathy, highlighting its clinical importance. Recent studies show TMEM65 acts as a mitochondrial Na+/Ca2+ exchanger in vitro. Here, we generated conditional Tmem65 knockout mice to define its role in neuromuscular tissues in vivo. Both whole-body and nervous system-specific Tmem65 knockouts exhibited severe growth retardation and seizure-associated sudden death at ~3 weeks, establishing TMEM65 as indispensable for neuronal function. Additionally, skeletal muscle-specific knockout produced adult-onset myopathy preceded by elevated mitochondrial Ca2+. Consistently, TMEM65 ablation caused loss of Na+-dependent mitochondrial Ca2+ export. Notably, blocking mitochondrial Ca2+ entry by mitochondrial calcium uniporter (MCU) knockout rescued the early lethality of whole-body Tmem65 ablation, extending lifespan from ~3 weeks to >1 year. These data reveal an essential physiological role for TMEM65 and suggest that modulating mitochondrial Ca2+ may offer therapeutic value for TMEM65 misexpression and other mitochondrial diseases associated with Ca2+ overload.
    DOI:  https://doi.org/10.1038/s41467-026-71761-w
  3. Nat Cell Biol. 2026 Apr 17.
      Metabolic processes shape ageing and longevity at multiple levels. Emerging evidence shows that many of these processes are orchestrated within and between cellular organelles. Organelles function not only as metabolic reactors but also as signalling hubs, and their coordination plays crucial roles in maintaining cellular homeostasis and promoting organismal fitness. Rather than acting in isolation, organelles engage in dynamic crosstalk through membrane contact sites, metabolite exchange and signalling interplay. In recent years, organelles have been increasingly recognized as critical regulators of ageing and longevity. Here we summarize age-related organellar changes, highlight organelle-mediated intra- and intercellular signalling communication in lifespan and healthspan regulation, and discuss the active roles of organelles in microbiome-host interactions and transgenerational inheritance in regulating longevity. We further outline how longevity-promoting interventions influence organelles, and provide perspectives on how future technological advances may further accelerate progress in this emerging research topic.
    DOI:  https://doi.org/10.1038/s41556-026-01927-7
  4. Stem Cell Rev Rep. 2026 Apr 13.
      
    Keywords:  Aging; Extracellular vesicles; Mitochondria; Neurodegeneration; Secretome; Senescence; Senotherapeutics
    DOI:  https://doi.org/10.1007/s12015-026-11117-5
  5. Trends Mol Med. 2026 Apr 14. pii: S1471-4914(26)00083-3. [Epub ahead of print]
      In a recent study in Cell, Liu et al. identify β-hydroxybutyrate as a practical metabolic adjuvant for CAR-T cells. By fueling the TCA cycle and reshaping transcriptional and epigenetic programs, this ketone body enhances proliferation, persistence, and tumor control, suggesting that metabolic supplementation may offer a simple route to more effective adoptive immunotherapy.
    Keywords:  CAR T cells; adoptive immunotherapy; immunometabolism; ketogenic diet; β-hydroxybutyrate
    DOI:  https://doi.org/10.1016/j.molmed.2026.04.001
  6. Nat Aging. 2026 Apr 16.
      Cellular senescence drives chronic sterile inflammation during aging via the senescence-associated secretory phenotype, yet the senescent cell types responsible are poorly defined. Macrophages share multiple features of senescence, including inflammatory secretion, yet whether macrophages can adopt a senescent state remains unclear. Here we identify p21⁺Trem2⁺ senescent macrophages as a major source of inflammaging, using primary mouse and human macrophage models of DNA damage and cholesterol-induced senescence characterized by multi-omic profiling. We found that senescent macrophages exhibit a distinctive p21-TREM2 expression profile and senescence-associated secretory phenotype, driven in part by type I interferon signaling via cytosolic mitochondrial DNA. We also found that senescent macrophage accumulation occurs in aging, metabolic dysfunction-associated steatotic liver disease mouse livers, and is enriched in human cirrhotic liver tissue. Finally, senolytic treatment targeting senescent macrophages reduced liver inflammation and steatosis in both aged mice and mice with metabolic dysfunction-associated steatotic liver disease. These findings establish macrophage senescence as a central driver of chronic inflammation in aging and metabolic liver disease, and a tractable therapeutic target.
    DOI:  https://doi.org/10.1038/s43587-026-01101-6