Cyclophilin a as a Mediator of Tissue Injure and Nephrotoxicity

Moscoso-Solorzano, G.; Mastroianni-Kirsztajn, G.

Nephrology Research and Reviews 4(2): 42-44

2012


DOI: 10.4081/nr.2012.e9
Accession: 068492335

Download citation:  
Text
  |  
BibTeX
  |  
RIS

Article/Abstract emailed within 0-6 h
Payments are secure & encrypted
Powered by Stripe
Powered by PayPal

Abstract
Cyclophilin A (Cyp A) belongs to the peptidyl-prolil isomerase (PPlase) family of proteins and it is also known as the cellular receptor for cyclosporine A (Cs A). Cs A binds to Cyp A and inhibits the PPIase activity, but the Cyp A-Cs A complex also binds to calcineurin that promotes the expression of genes encoding cytokines and other proteins required for immune response. In addition, the polymorphism variation of Cyp A promoter seems to have an influence on the expression of Cyp A in in vitro studies. Cyp A was also implicated in inflammatory processes (such as, among others, those observed in rheumatoid arthritis, atherosclerotic disease, nephrotoxicity) and it can be secreted by cells in response to inflammatory stimuli. Cyp A can also have a role in the molecular mechanisms by which Cs A induces nephroxicity but these remain poorly understood. Recent studies suggest that Cs A inhibition of Cyp A PPlase activity is a possible mechanism of this drug toxicity. In addition, Cyp A overexpression could be protective against Cs A nephrotoxicity. Finally, the putative common mechanism by which Cyp A could be involved in Cs A nephrotoxicity and tissue injury is related to its proinflammatory effects in cells.