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心肌能够应对内外环境改变而发生重塑。失重/模拟失重等去负荷条件可导致心肌萎缩、心脏功能下降。从系统和细胞分子层面揭示失重/模拟失重造成心肌萎缩的机制对于航天飞行后心血管功能紊乱的对抗研究至关重要。失重/模拟失重导致机体血流动力负荷下降、代谢需求降低和神经内分泌变化;同时导致包括钙相关信号、NF-κB通路、ERK通路、泛素-蛋白酶体途径以及自噬等通路的改变,上述变化在心肌萎缩的发生发展过程中发挥着关键调控作用。本文从系统和细胞分子层面对失重/模拟失重引起心肌萎缩的发生机制进行综述。
Myocardium can be reshaped in response to changes in the environment. Weight loss / simulated weight loss and other load conditions can lead to myocardial atrophy, decreased cardiac function. Mechanisms to reveal myocardial atrophy due to weightlessness / simulated weight loss at the systemic and cellular molecular level Research on confrontation of cardiovascular dysfunctions after aerospace flight is crucial. Loss of weight / simulated weight loss leads to decreased hemodynamic load, decreased metabolic requirements, and neuroendocrine changes; at the same time, changes in pathways including calcium-related signaling, NF-κB pathway, ERK pathway, ubiquitin- Changes in the occurrence and development of myocardial atrophy play a key regulatory role. This article reviews the mechanism of cardiac atrophy caused by weightlessness / simulated weightlessness at the systemic and cellular level.