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Cellular senescence and the senescent secretory phenotype: therapeutic opportunities

Tamara Tchkonia1, Yi Zhu, Jan van Deursen

  • 1Robert and Arlene Kogod Center on Aging, Mayo Clinic, Rochester, Minnesota 55905, USA.

The Journal of Clinical Investigation
|March 5, 2013
PubMed

Insights

Aging is a modifiable risk factor for chronic diseases. Targeting cellular senescence and its associated inflammatory pathways offers a promising strategy to delay multiple age-related conditions and improve healthspan.

Area of Science:

  • Gerontology and cellular biology.
  • Immunology and chronic disease research.

Background:

  • Aging is the primary risk factor for numerous chronic diseases, driving significant healthcare costs.
  • Chronic diseases and frailty are major burdens in developed nations, linked to aging processes.

Purpose of the Study:

  • To explore aging as a modifiable risk factor for age-related diseases.
  • To review the role of cellular senescence and the senescence-associated secretory phenotype (SASP) in aging and disease.
  • To discuss therapeutic strategies targeting senescent cells and SASP for clinical intervention.

Main Methods:

  • Review of existing literature on aging mechanisms, cellular senescence, and SASP.
  • Analysis of the association between senescence, SASP, chronic diseases, and frailty.
  • Exploration of current and potential therapeutic interventions targeting senescent cells.

Main Results:

  • Cellular senescence, characterized by the SASP, contributes to chronic inflammation.
  • The SASP is implicated in the pathogenesis of various age-related chronic diseases and frailty.
  • Targeting senescent cells presents a viable therapeutic avenue for age-related conditions.

Conclusions:

  • Modulating fundamental aging mechanisms, specifically cellular senescence, may delay multiple chronic diseases simultaneously.
  • Therapeutic strategies focused on senescent cells and SASP hold promise for improving healthspan and treating age-related pathologies.
  • Further research into clinical interventions targeting senescence is warranted.

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