心脏衰竭的分子机制:致命的倒退?

Manami Katoh, Jin Komuro, Shunsuke Inoue, Yukiteru Nakayama, I. Komuro
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引用次数: 0

摘要

心力衰竭(HF)是最常见的死亡原因之一,由于人口老龄化,全世界心力衰竭患者的人数正在不断增加。许多研究人员以心肌细胞为重点,对心力衰竭的发病机制进行了广泛研究,但其复杂的病理生理学仍有待阐明。构成心脏的细胞中,非心肌细胞占 70% 以上,而且非心肌细胞与心肌细胞之间存在密切交流,这表明非心肌细胞可能在心房颤动的发病过程中扮演着关键角色。神经体液因素,如自律神经和激素,调节着心脏的功能。相反,心脏通过血液灌流影响许多其他器官,这凸显了器官间交流的重要性。这篇综述讨论了非心肌细胞以及心脏与其他器官之间的器官间通讯在高房颤发展过程中的作用,而这一主题尚未得到广泛探讨。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Molecular Mechanisms of the Failing Heart: A Fatal Regression?
Heart failure (HF) is one of the most common causes of death, and the number of HF patients is increasing worldwide due to population ageing. The pathogenesis of HF has been extensively studied by many researchers with a focus on cardiomyocytes, but its complex pathophysiology has yet to be elucidated. Non-cardiomyocytes account for >70% of the cells that comprise the heart, and there is close communication between non-cardiomyocytes and cardiomyocytes, suggesting that non-cardiomyocytes might play a pivotal role in the development of HF. Neurohumoral factors, such as the autonomic nerves and hormones, regulate the heart’s function. Conversely, the heart affects many other organs through blood perfusion, underscoring the importance of interorgan communication. This review discusses the role of non-cardiomyocytes and interorgan communication between the heart and other organs in the development of HF, a topic that has not been extensively explored.
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