脓毒症引起的心功能障碍:线粒体和能量代谢。

IF 2.8 Q2 CRITICAL CARE MEDICINE
Xueting Yu, Jie Gao, Chunxiang Zhang
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引用次数: 0

摘要

脓毒症是一种由宿主对感染反应失调引起的危及生命的多器官功能障碍综合征,对全球卫生保健构成了重大挑战。脓毒症引起的心肌功能障碍(SIMD)是脓毒症的常见并发症,由于其高能量需求和低代偿储备,显著增加了死亡率。线粒体损伤而非细胞凋亡表明心肌能量代谢紊乱是一个重要的病理生理机制。因此,我们系统地回顾了SIMD中能量代谢功能障碍的机制,包括心肌细胞能量代谢底物的改变、兴奋-收缩耦合过程、线粒体功能障碍、线粒体自噬和生物发生,并总结了其中潜在的治疗靶点。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Sepsis-induced cardiac dysfunction: mitochondria and energy metabolism.

Sepsis-induced cardiac dysfunction: mitochondria and energy metabolism.

Sepsis is a life-threatening multi-organ dysfunction syndrome caused by dysregulated host response to infection, posing a significant global healthcare challenge. Sepsis-induced myocardial dysfunction (SIMD) is a common complication of sepsis, significantly increasing mortality due to its high energy demands and low compensatory reserves. The substantial mitochondrial damage rather than cell apoptosis in SIMD suggests disrupted cardiac energy metabolism as a crucial pathophysiological mechanism. Therefore, we systematically reviewed the mechanisms underlying energy metabolism dysfunction in SIMD, including alterations in myocardial cell energy metabolism substrates, excitation-contraction coupling processes, mitochondrial dysfunction, and mitochondrial autophagy and biogenesis, summarizing potential therapeutic targets within them.

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来源期刊
Intensive Care Medicine Experimental
Intensive Care Medicine Experimental CRITICAL CARE MEDICINE-
CiteScore
5.10
自引率
2.90%
发文量
48
审稿时长
13 weeks
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