Cellular senescence

Byaibio

Cellular senescence is an irreversible cell-cycle arrest state and a hallmark of biological aging, with major roles in neurodegenerative disorders and diabetic kidney disease. It is implicated in brain aging and neurodegeneration, and in diabetic kidney disease it is described as a recognized driver of pathogenesis and a therapeutic focus for senotherapeutic approaches. Recent studies also link senescence to skin biology, where chlorogenic acid and taurine were reported to reduce skin cellular senescence, and to mitochondrial homeostasis, where ginsenoside Rg5 antagonized senescence via the KAT8-CISD2 axis. Overall, the literature highlights senescence as a mechanistically diverse aging program influenced by mitochondrial dysfunction, autophagy, and bioactive compounds such as ginsenosides. The entry also notes that ginsenosides regulate cellular senescence in aging mechanisms, consistent with their broader functional-food and longevity research.

Neurodegeneration

  • Cellular senescence is described as a crucial contributor to the development of neurodegenerative disorders and brain aging. (PMID:41811567)
  • A 2026 Cellular and Molecular Neurobiology review linked interplay between autophagy, cellular senescence, and brain aging to neuroprotective implications of intermittent fasting. (PMID:41811567)

Diabetic kidney disease

  • Cellular senescence is an irreversible cell-cycle arrest state recognized as a driver of diabetic kidney disease pathogenesis. (PMID:41581730)
  • A 2026 Kidney International review discussed senotherapeutics as a therapeutic focus for reducing senescence burden in DKD. (PMID:41581730)
  • Regenerative, cell-based therapies were highlighted as part of the broader senescence-targeting strategy in DKD. (PMID:41581730)

Skin aging and protective compounds

  • Transcriptomic profiling showed that chlorogenic acid and taurine treatment in human skin cells provides insight into cellular senescence mechanisms. (PMID:41938013)
  • Chlorogenic acid is reported to reduce skin cellular senescence. (PMID:41938013)
  • Taurine is also reported to reduce skin cellular senescence. (PMID:41938013)

Mitochondrial dysfunction and ginsenosides

  • Ginsenoside Rg5 was reported to antagonize senescence by targeting the KAT8-CISD2 axis and maintaining mitochondrial homeostasis. (PMID:41687537)
  • The abstract described senescence as a state driven by mitochondrial dysfunction, supporting a mitochondria-centered mechanism. (PMID:41687537)
  • Dietary ginsenosides were reviewed as bioactive compounds with longevity-related potential and functional food applications. (PMID:41945483)
  • Ginsenosides are described as regulating cellular senescence in aging mechanisms. (PMID:41945483)