bims-cesemi Biomed News
on Cellular senescence and mitochondria
Issue of 2025–11–16
six papers selected by
Julio Cesar Cardenas, Universidad Mayor



  1. Nat Metab. 2025 Nov 12.
      Skeletal muscle wasting is a defining feature of cancer cachexia, a multifactorial syndrome that drastically compromises patient quality of life and treatment outcomes. Mitochondrial dysfunction is a major contributor to skeletal muscle wasting in cancer cachexia, yet the upstream molecular drivers remain elusive. Here we show that cancer impairs the activity of cAMP-dependent protein kinase A (PKA) and of its transcriptional effector CREB1 in skeletal muscle, ultimately contributing to the downregulation of a core transcriptional network that supports mitochondrial integrity and function. The restoration of cAMP-PKA-CREB1 signalling through pharmacological inhibition of the cAMP-hydrolysing phosphodiesterase 4 (PDE4) rescues the expression of mitochondrial-related genes, improves mitochondrial function and mitigates skeletal muscle wasting in male mice. Altogether, our data identify tumour-induced suppression of the cAMP-PKA-CREB1 axis as a central mechanism contributing to mitochondrial dysfunction in skeletal muscle during cancer cachexia. Furthermore, these findings highlight PDE4, particularly the PDE4D isoform, as a potential therapeutic target to preserve muscle mitochondrial function and counteract muscle wasting in cancer cachexia.
    DOI:  https://doi.org/10.1038/s42255-025-01397-5
  2. Nat Commun. 2025 Nov 10. 16(1): 9868
      Skeletal muscles, which constitute 40-50% of body mass, regulate whole-body energy expenditure and glucose and lipid metabolism. Peroxisomes are dynamic organelles that play a crucial role in lipid metabolism and clearance of reactive oxygen species, however their role in skeletal muscle remains poorly understood. To clarify this issue, we generated a muscle-specific transgenic mouse line with peroxisome import deficiency through the deletion of peroxisomal biogenesis factor 5 (Pex5). Here, we show that Pex5 inhibition results in impaired lipid metabolism, reduced muscle force and exercise performance. Moreover, mitochondrial structure, content, and function are also altered, accelerating the onset of age-related structural defects, neuromuscular junction degeneration, and muscle atrophy. Consistent with these observations, we observe a decline in peroxisomal content in the muscles of control mice undergoing natural aging. Altogether, our findings show the importance of preserving peroxisomal function and their interplay with mitochondria to maintain muscle health during aging.
    DOI:  https://doi.org/10.1038/s41467-025-64833-w
  3. Nature. 2025 Nov;647(8089): S8-S11
      
    Keywords:  Ageing; Alzheimer's disease; Research data
    DOI:  https://doi.org/10.1038/d41586-025-03525-3
  4. Age Ageing. 2025 Oct 30. pii: afaf327. [Epub ahead of print]54(11):
      
    Keywords:  activity; exercise; fitness; healthy ageing; older people
    DOI:  https://doi.org/10.1093/ageing/afaf327
  5. Science. 2025 Nov 13. 390(6774): 664-665
      Science historian Nathaniel Comfort reflects on the "most famous scientist of the 20th century, and the most infamous of the 21st".
    DOI:  https://doi.org/10.1126/science.aed8420