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Mechanisms of cyclosporine-induced renal cell apoptosis: a systematic review

Zheng Xiao1, Juan Shan, Chengwen Li

  • 1Key Laboratory of Transplant Engineering and Immunology of the Ministry of Health of China, West China Hospital, Sichuan University, Chengdu, PR China.

American Journal of Nephrology
|January 9, 2013
PubMed
Abstract

Insights

Chronic cyclosporine A (CsA) nephrotoxicity causes kidney dysfunction through renal cell apoptosis. This review identifies five key pathways, including oxidative stress and endoplasmic reticulum stress, highlighting activated caspases as a common mechanism.

Area of Science:

  • Nephrology
  • Toxicology
  • Molecular Biology

Background:

  • Chronic cyclosporine A (CsA) nephrotoxicity (CCN) is a significant cause of chronic renal dysfunction.
  • Currently, no effective clinical interventions exist for CCN.

Purpose of the Study:

  • To elucidate the in vivo mechanisms of renal cell apoptosis in chronic cyclosporine A nephrotoxicity.
  • To identify potential therapeutic targets for CCN.

Main Methods:

  • Systematic review of in vivo studies on CsA-induced renal cell apoptosis.
  • Searched Medline, Embase, and ISI databases (1966-July 2010).
  • Studies evaluated for quality using in vivo standards and data extracted via PICOS.

Main Results:

  • Renal cell apoptosis is a key feature of CCN and a factor in renal dysfunction.
  • CsA induces apoptosis via upregulation of Fas/Fas ligand, downregulation of Bcl-2/Bcl-XL, and increased caspases.
  • CsA also induces oxidative stress, endoplasmic reticulum stress, and impairs urine concentration mechanisms.
  • Blocking the angiotensin II type 1 receptor with losartan significantly decreased CsA-induced apoptosis.

Conclusions:

  • In vivo mechanisms of CCN are complex, involving at least five distinct pathways.
  • Activated caspases represent a common intracellular pathway mediating apoptosis in CCN.
  • These findings offer potential intervention points for CCN, requiring further investigation.

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