Literature DB >> 27927651

DNA repair in ischemic acute kidney injury.

Jeffrey D Pressly1, Frank Park2.   

Abstract

Ischemia-reperfusion injury (IRI) is a common cause of acute kidney injury leading to an induction of oxidative stress, cellular dysfunction, and loss of renal function. DNA damage, including oxidative base modifications and physical DNA strand breaks, is a consequence of renal IRI. Like many other organs in the body, a redundant and highly conserved set of endogenous repair pathways have evolved to selectively recognize the various types of cellular DNA damage and combat its negative effects on cell viability. Severe damage to the DNA, however, can trigger cell death and elimination of the injured tubular epithelial cells. In this minireview, we summarize the state of the current field of DNA damage and repair in the kidney and provide some expected and, in some cases, unexpected effects of IRI on DNA damage and repair in the kidney. These findings may be applicable to other forms of acute kidney injury and could provide new opportunities for renal research.
Copyright © 2017 the American Physiological Society.

Entities:  

Keywords:  DNA repair; TRIP13; acute kidney injury; tubular epithelial cells

Mesh:

Year:  2016        PMID: 27927651      PMCID: PMC5407066          DOI: 10.1152/ajprenal.00492.2016

Source DB:  PubMed          Journal:  Am J Physiol Renal Physiol        ISSN: 1522-1466


  52 in total

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