mTOR Signaling from Cellular Senescence to Organismal Aging

Shaohua Xu1, Ying Cai2, Yuehua Wei3

  • 1Gladstone Institute of Cardiovascular Disease, University of California San Francisco, San Francisco, CA94102, USA.

Aging and Disease
|August 12, 2014
PubMed

Insights

Inhibiting the target of rapamycin (TOR) pathway with rapamycin extends lifespan and delays aging-related diseases in mice. This review explores how targeting cellular senescence via mTOR inhibition may unlock longevity secrets.

Area of Science:

  • Gerontology
  • Cellular Biology
  • Molecular Biology

Background:

  • The target of rapamycin (TOR) pathway is implicated in promoting aging across diverse organisms.
  • Rapamycin treatment in mice extends lifespan and mitigates age-related diseases, but mechanisms remain unclear.
  • Cellular senescence is a hallmark of aging, making it a key model for studying aging mechanisms.

Purpose of the Study:

  • To review the relationship between mTOR signaling and cellular senescence.
  • To explore how inhibiting mTOR impacts longevity and age-related diseases through cellular senescence.
  • To discuss the dual role of senescence in human diseases and interpret experimental findings.

Main Methods:

  • Literature review focusing on mTOR signaling and cellular senescence.
  • Analysis of studies investigating rapamycin's effects on aging and senescence.
  • Examination of the interplay between mTOR pathways and senescence markers.

Main Results:

  • mTOR inhibition influences cellular senescence, a key factor in aging.
  • Understanding senescence in the context of mTOR signaling is crucial for comprehending organismal aging.
  • Senescence exhibits complex, sometimes opposing, roles in various human diseases.

Conclusions:

  • Targeting cellular senescence via mTOR inhibition presents a promising avenue for promoting longevity.
  • Further research is needed to fully elucidate the mechanisms linking mTOR, senescence, and aging.
  • Careful interpretation of data is essential due to the multifaceted roles of senescence in disease.

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