Replicative senescence in kidney aging, renal disease, and renal transplantation

Maarten Naesens1

  • 1Department of Nephrology and Renal Transplantation, University Hospitals Leuven, Belgium. maarten.naesens@uzleuven.be

Discovery Medicine
|February 1, 2011
PubMed

Insights

Cellular senescence, involving pathways like p53 and p16, impacts kidney disease and transplant outcomes. While traditionally viewed as aging

Area of Science:

  • Gerontology and Nephrology
  • Cellular Biology and Molecular Mechanisms

Background:

  • Cellular senescence is a key aging hallmark.
  • Replicative senescence pathways (p53, p16) are implicated in kidney disease and transplantation outcomes, irrespective of chronological age.

Purpose of the Study:

  • To review molecular mechanisms of cellular senescence.
  • To correlate senescence theories with kidney aging, disease, and allograft outcomes.

Main Methods:

  • Literature review and synthesis of current concepts.
  • Correlation of in vivo senescence biology with clinical and preclinical data.

Main Results:

  • Senescence has complex in vivo biology, challenging its view as solely detrimental.
  • Senescence may limit renal fibrosis, as suggested by animal studies.

Conclusions:

  • Senescence's role in kidney aging and disease is multifaceted.
  • Further investigation is needed to clarify senescence's active or bystander role in human renal fibrogenesis and atrophy.

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