肝脂肪变性对肝缺血再灌注生物能量功能的影响:系统综述

M. Chu, A. Dare, A. Bartlett, A. Phillips, A. Hickey
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引用次数: 1

摘要

背景:肝脂肪变性对肝缺血再灌注损伤(IRI)后生物能量学的影响仍然存在争议,其结果的报道也不尽相同。大量的研究已经发表,探讨肝脂肪变性和肝IRI后细胞生物能量学之间的关系。本文系统地评价了这些研究。方法:对Medline和Embase数据库(1946年1月至2012年6月)进行电子检索,以选择报告IRI动物模型或肝脂肪变性患者相关结果的研究。结果:共纳入489篇文献,其中63篇动物研究符合预定标准,纳入本研究。肝脂肪变性的动物模型类型、持续时间、IRI类型和组织学描述存在较大差异。生物能量损伤似乎增加了脂肪变性肝脏对IRI的易感性。最常见的损伤是IRI后氧化应激增加导致三磷酸腺苷恢复减少。线粒体功能受损在脂肪肝对IRI的易感性中起关键作用。结论:肝脂肪变性为> - 30%的动物在IRI后的预后较差。尽管不同的实验模型存在局限性,组织学描述也不一致,但线粒体功能和生物能量学受损似乎是脂肪变性肝脏对IRI耐受性降低的重要介质。未来的研究需要一致性和临床相关性,以进一步提高我们对这一问题的理解。
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Effect of Hepatic Steatosis on Bioenergetic Function During HepaticIschemia-reperfusion: A Systematic Review
Background: The impact of hepatic steatosis on bioenergetics following hepatic ischemia-reperfusion injury (IRI) remains controversial and is associated with variable reports on its outcome. Large numbers of studies have been published examining the relationship between hepatic steatosis and cellular bioenergetics following hepatic IRI. This sys- tematic review evaluates these studies. Methods: An electronic search of the Medline and Embase databases (January 1946 to June 2012) was performed to select studies that reported relevant outcomes in animal models or patients with hepatic steatosis subjected to IRI. Results: A total of 489 articles were identified, of which 63 animal studies met the predefined criteria and were included in the study. There was large variation in the type of animal model, duration and type of IRI utilized and histological de- scription of hepatic steatosis. Bioenergetic impairments appear to increase the susceptibility of steatotic livers to IRI. The most common impairment was decreased adenosine triphosphate recovery with increased oxidative stress following IRI. Impaired mitochondrial function play a key role in the susceptibility of steatotic livers to IRI. Conclusions: Animals with >30% hepatic steatosis have been shown to have poor outcome following IRI. Despite limita- tions of different experimental models and inconsistency in histological description, impaired mitochondrial function and bioenergetics appear to be important mediators in the decreased tolerance of steatotic livers to IRI. Future studies need to be consistent and clinically relevant to further improve our understanding of this issue.
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