Yu Xueting, Gao Jie, Zhang Chunxiang
Key Laboratory of Medical Electrophysiology, Ministry of Education, Institute of Cardiovascular Research, the Affiliated Hospital of Southwest Medical University, Southwest Medical University, Luzhou, Sichuan, China.
Department of Cardiology, Institute of Cardiovascular Research, the Affiliated Hospital of Southwest Medical University, Southwest Medical University, Luzhou, Sichuan, China.
Intensive Care Med Exp. 2025 Feb 18;13(1):20. doi: 10.1186/s40635-025-00728-w.
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.
脓毒症是一种由宿主对感染的反应失调引起的危及生命的多器官功能障碍综合征,给全球医疗保健带来了重大挑战。脓毒症诱导的心肌功能障碍(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。SIMD中大量的线粒体损伤而非细胞凋亡表明心脏能量代谢紊乱是关键的病理生理机制。因此,我们系统地综述了SIMD中能量代谢功能障碍的潜在机制,包括心肌细胞能量代谢底物的改变、兴奋-收缩偶联过程、线粒体功能障碍以及线粒体自噬和生物发生,并总结了其中的潜在治疗靶点。