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Autophagy in chronic stress induced atherosclerosis

机译:慢性应激诱导动脉粥样硬化的自噬

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摘要

Atherosclerosis, a complex multifactorial disease, is the leading cause of acute cardiovascular events. Substantial evidence confirms that chronic stress plays a pivot role in the occurrence and development of atherosclerosis, but the specific mechanism remains unclear. Autophagy serves as a safeguard mechanism for sustaining cellular homeostasis via eliminating unnecessary or/and harmful components, and damaged organelles in response to various stress. An increasing number of studies indicate that autophagy plays vital roles in the development of atherosclerosis. Therefore, understanding the role of chronic stress in the regulation of autophagy may provide new insight into prevention and treatment atherosclerotic disease, especially with respect to emerging targeted therapy. In present review, we focus on changes in autophagic function under chronic stress and its relationship to atherosclerosis.
机译:动脉粥样硬化,复杂的多学会疾病,是急性心血管事件的主要原因。 实质性证据证实,慢性应力在动脉粥样硬化的发生和发展中起着枢轴作用,但具体机制仍然不清楚。 自噬是通过消除不必要的或/和有害的组分,以及响应各种压力而受到不必要的或/和有害的组件,作为维持细胞稳态的保障机制。 越来越多的研究表明,自噬在动脉粥样硬化的发展中起着重要作用。 因此,了解慢性胁迫在自噬调节中的作用可能会对预防和治疗动脉粥样硬化疾病提供新的洞察力,特别是对于出现的靶向治疗。 在本综述中,我们专注于慢性胁迫下自噬功能的变化及其与动脉粥样硬化的关系。

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