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Updated: Jan 26, 2026

Techniques to Induce and Quantify Cellular Senescence
06:51

Techniques to Induce and Quantify Cellular Senescence

Published on: May 1, 2017

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Cellular Senescence in the Kidney

Marie-Helena Docherty1, Eoin D O'Sullivan1,2, Joseph V Bonventre3

  • 1Department of Renal Medicine, Royal Infirmary of Edinburgh, Edinburgh, UK.

Journal of the American Society of Nephrology : JASN
|April 20, 2019
PubMed

Insights

Senescent cells, linked to aging and kidney injury, drive organ dysfunction. Targeting these cells may extend lifespan and treat kidney disease.

Area of Science:

  • Cellular senescence
  • Renal pathophysiology
  • Aging research

Background:

  • Senescent cells exhibit permanent growth arrest and a distinct secretory phenotype.
  • These cells accumulate in aging and injured kidneys, impacting organ function.
  • Senescence plays roles in development, repair, and tumor suppression.

Purpose of the Study:

  • To review current knowledge on senescence in the human and experimental kidney.
  • To examine the dual role of senescence in kidney homeostasis and disease.
  • To discuss senolytic therapies for renal conditions.

Main Methods:

  • Literature review of senescence in kidney disease.
  • Analysis of experimental models and human studies.
  • Synthesis of evidence on senescent cell manipulation.

Main Results:

  • Senescence is crucial for normal kidney development and homeostasis.
  • Chronic senescent cell accumulation drives maladaptive repair, fibrosis, and transplant failure.
  • Depletion of senescent cells shows promise in extending lifespan and delaying age-related diseases.

Conclusions:

  • Senescence is a key factor in kidney aging and disease progression.
  • Targeting senescent cells represents a promising therapeutic strategy for kidney disorders.
  • Further research is needed to address uncertainties and optimize senolytic therapies for renal applications.
Keywords:
acute renal failurechronic kidney diseasefibrosiskidney developmentprogression of renal failure

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