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Short and dysfunctional telomeres sensitize the kidneys to develop fibrosis

Sarita Saraswati1, Paula Martínez1, Osvaldo Graña-Castro2

  • 1Telomeres and Telomerase Group, Molecular Oncology Program, Spanish National Cancer Research Centre, Madrid, Spain.

Nature Aging
|April 28, 2023
PubMed

Insights

Short telomeres accelerate kidney fibrosis and epithelial-to-mesenchymal transition (EMT) in mice. Telomere dysfunction contributes to age-associated renal fibrosis by impacting the EMT program.

Area of Science:

  • Nephrology
  • Cell Biology
  • Aging Research

Background:

  • Telomere shortening is a key aging indicator.
  • Mutations in telomere-related genes cause telomere syndromes, leading to tissue regeneration loss and fibrosis.
  • The role of telomere dysfunction in age-associated kidney fibrosis is not fully understood.

Purpose of the Study:

  • To investigate the contribution of telomere shortening and dysfunction to kidney fibrosis.
  • To explore the impact of telomere attrition on the epithelial-to-mesenchymal transition (EMT) program in renal fibrosis.

Main Methods:

  • Generated mouse models of kidney fibrosis by inducing telomere shortening (telomerase deficiency + folic acid) or telomere dysfunction (Trf1 deletion in kidneys).
  • Assessed kidney fibrosis development and EMT activation in response to telomere-related insults.

Main Results:

  • Short telomeres sensitized kidneys to folic acid-induced fibrosis.
  • Telomere shortening exacerbated the EMT program in kidney fibrosis models.
  • Conditional deletion of Trf1 in kidneys induced fibrosis and EMT.

Conclusions:

  • Telomere shortening and dysfunction can promote kidney fibrosis.
  • Telomere attrition influences the EMT program, contributing to age-associated renal fibrosis.
  • Findings highlight telomeres as potential targets for treating kidney fibrosis.

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