Mitochondrial Mechanisms in Septic Cardiomyopathy.

Mitochondrial Mechanisms in Septic Cardiomyopathy.
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脓毒症心肌病的线粒体机制。

DOI:
10.3390/ijms160817763
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发表时间:
2015-08-03
影响因子:
5.6
通讯作者:
Bugger H
Bugger H
中科院分区:
生物学2区
文献类型:
--
作者:
Cimolai MC;Alvarez S;Bode C;Bugger H

文献摘要

被引文献

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脓毒症是对感染的免疫和炎症反应的表现,最终可能导致多器官衰竭。尽管到目前为止已经使用的治疗策略,败血症和感染性休克仍然是危重患者死亡的主要原因。心肌功能障碍是严重脓毒症的常见并发症,也称为感染性心肌病,可进展为右室和左室泵衰竭。脓毒症心肌功能障碍可能涉及多种物质和机制,包括毒素、细胞因子、一氧化氮、补体激活、细胞凋亡和能量代谢紊乱等。然而,败血症心肌病确切的潜在分子机制及其在发病机制中的意义仍不完全清楚。感染性心肌病中一个被广泛研究的异常是线粒体功能障碍,它可能通过导致心肌能量耗竭而导致心功能障碍。感染性心肌病导致线粒体功能障碍的机制有很多,但仍有争议的是某些机制损害了线粒体功能,还是恢复了线粒体功能。该综述的目的是讨论感染性心肌病线粒体功能障碍的原因和/或可能是对线粒体功能障碍的适应性反应的线粒体机制。
Sepsis is the manifestation of the immune and inflammatory response to infection that may ultimately result in multi organ failure. Despite the therapeutic strategies that have been used up to now, sepsis and septic shock remain a leading cause of death in critically ill patients. Myocardial dysfunction is a well-described complication of severe sepsis, also referred to as septic cardiomyopathy, which may progress to right and left ventricular pump failure. Many substances and mechanisms seem to be involved in myocardial dysfunction in sepsis, including toxins, cytokines, nitric oxide, complement activation, apoptosis and energy metabolic derangements. Nevertheless, the precise underlying molecular mechanisms as well as their significance in the pathogenesis of septic cardiomyopathy remain incompletely understood. A well-investigated abnormality in septic cardiomyopathy is mitochondrial dysfunction, which likely contributes to cardiac dysfunction by causing myocardial energy depletion. A number of mechanisms have been proposed to cause mitochondrial dysfunction in septic cardiomyopathy, although it remains controversially discussed whether some mechanisms impair mitochondrial function or serve to restore mitochondrial function. The purpose of this review is to discuss mitochondrial mechanisms that may causally contribute to mitochondrial dysfunction and/or may represent adaptive responses to mitochondrial dysfunction in septic cardiomyopathy.