自噬
细胞生物学
生物
平衡
昼夜节律
程序性细胞死亡
机制(生物学)
神经科学
ULK1
生物化学
细胞凋亡
安普克
哲学
认识论
蛋白激酶A
磷酸化
作者
Inna Rabinovich-Nikitin,Matthew Love,Lorrie A. Kirshenbaum
标识
DOI:10.1016/j.bbadis.2022.166354
摘要
Autophagy is a vital cellular mechanism that controls the removal of damaged or dysfunctional cellular components. Autophagy allows the degradation and recycling of damaged proteins and organelles into their basic constituents of amino acids and fatty acids for cellular energy production. Under basal conditions, autophagy is essential for the maintenance of cell homeostasis and function. However, during cell stress, excessive activation of autophagy can be destructive and lead to cell death. Autophagy plays a crucial role in the cardiovascular system and helps to maintain normal cardiac function. During ischemia- reperfusion, autophagy can be adaptive or maladaptive depending on the timing and extent of activation. In this review, we highlight the molecular mechanisms and signaling pathways that underlie autophagy in response to cardiac stress and therapeutic approaches to modulate autophagy by pharmacological interventions. Finally, we also discuss the intersection between autophagy and circadian regulation in the heart. Understanding the mechanisms that underlie autophagy following cardiac injury can be translated to clinical cardiology use toward improved patient treatment and outcomes.
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