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suck abstract from ncbi


10.1152/ajprenal.00492.2016

http://scihub22266oqcxt.onion/10.1152/ajprenal.00492.2016
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C5407066!5407066!27927651
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suck abstract from ncbi

pmid27927651      Am+J+Physiol+Renal+Physiol 2017 ; 312 (4): F551-5
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  • DNA repair in ischemic acute kidney injury #MMPMID27927651
  • Pressly JD; Park F
  • Am J Physiol Renal Physiol 2017[Apr]; 312 (4): F551-5 PMID27927651show ga
  • 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.
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