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Podocyte Ercc1 is indispensable for glomerular integrity.

Eriko Yoshida Hama1, Ran Nakamichi1, Akihito Hishikawa1

  • 1Division of Nephrology, Endocrinology and Metabolism, Department of Internal Medicine, Keio University School of Medicine, Tokyo, Japan.

Biochemical and Biophysical Research Communications
|March 1, 2024
PubMed
Summary

Podocyte ERCC1 (excision repair cross-complementation group 1) is crucial for kidney health. Its deficiency accelerates aging and causes kidney failure by increasing DNA damage and inflammation.

Keywords:
AgingDNA damageERCC1Podocytes

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Area of Science:

  • Nephrology
  • Molecular Biology
  • Aging Research

Background:

  • Increasing life expectancy leads to a rise in age-related kidney diseases.
  • Chronic kidney disease (CKD) is linked to aging, potentially accelerating the aging process.
  • The role of DNA repair in kidney aging and disease requires further investigation.

Purpose of the Study:

  • To investigate the role of podocyte ERCC1 (excision repair cross-complementation group 1) in maintaining glomerular integrity.
  • To explore the impact of podocyte ERCC1 deficiency on aging markers and systemic inflammation.
  • To assess the potential of ERCC1 gene transfer in mitigating kidney damage.

Main Methods:

  • Generation of podocyte-specific ERCC1-knockout mice.
  • Analysis of kidney function, glomerular histology, and DNA damage markers (SSBs and DSBs).
  • Evaluation of T-cell senescence (CD44+CD8+ memory T cells) and senescence-associated secretory phenotype (SASP) factors.
  • Assessment of ERCC1 expression and DNA damage in aging mice and human kidney samples.

Main Results:

  • Podocyte ERCC1 knockout led to severe proteinuria, glomerulosclerosis, renal failure, and increased glomerular DNA breaks.
  • ERCC1 gene transfer ameliorated proteinuria and glomerulosclerosis, reducing DNA damage.
  • ERCC1 deficiency induced T-cell senescence and elevated SASP factors systemically and in multiple organs.
  • Accumulation of DNA breaks, particularly SSBs, was observed in glomeruli of aging mice and human patients.

Conclusions:

  • Podocyte ERCC1 is essential for repairing DNA damage and maintaining glomerular structure.
  • ERCC1 deficiency in podocytes accelerates aging phenotypes, including T-cell senescence and systemic inflammation.
  • Targeting ERCC1 may offer therapeutic potential for age-related kidney diseases and associated inflammation.