Abstract | SIGNIFICANCE: Hepatic ischemia-reperfusion (IR) injury results from the temporary deprivation of hepatic blood supply and is a common side effect of major liver surgery (i.e., transplantation or resection). IR injury, which in most severe cases culminates in acute liver failure, is particularly pronounced in livers that are affected by non-alcoholic fatty liver disease ( NAFLD). In NAFLD, fat-laden hepatocytes are damaged by chronic oxidative/nitrosative stress (ONS), a state that is acutely exacerbated during IR, leading to extensive parenchymal damage. RECENT ADVANCES: CRITICAL ISSUES: Despite the fact that ONS mediates both NAFLD and IR injury, the interplay between the two conditions has never been described in detail. An integrative overview of the pathophysiology of NAFLD that renders steatotic hepatocytes more vulnerable to IR injury is therefore presented in the context of ONS. FUTURE DIRECTIONS: Effective methods should be devised to alleviate ONS and the consequences thereof in NAFLD before surgery in order to improve resilience of fatty livers to IR injury.
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Authors | Megan J Reiniers, Rowan F van Golen, Thomas M van Gulik, Michal Heger |
Journal | Antioxidants & redox signaling
(Antioxid Redox Signal)
Vol. 21
Issue 7
Pg. 1119-42
(Sep 01 2014)
ISSN: 1557-7716 [Electronic] United States |
PMID | 24294945
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't, Review)
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Chemical References |
- Reactive Nitrogen Species
- Reactive Oxygen Species
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Topics |
- Animals
- Fatty Liver
(metabolism, pathology)
- Hepatocytes
(metabolism, pathology)
- Humans
- Reactive Nitrogen Species
(metabolism)
- Reactive Oxygen Species
(metabolism)
- Reperfusion Injury
(metabolism, pathology)
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