脑缺血早期钙毒性诱导自噬细胞死亡和溶酶体降解的内在机制

IF 1.4 Q3 ANATOMY & MORPHOLOGY
Anatomy & Cell Biology Pub Date : 2024-06-30 Epub Date: 2024-04-29 DOI:10.5115/acb.24.003
Jirakhamon Sengking, Pasuk Mahakkanukrauh
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引用次数: 0

摘要

脑缺血是全球致残和致死的重要原因,是脑血管供应障碍的一种。在早期阶段,谷氨酸兴奋毒性和高水平的细胞内钙(Ca2+)是主要过程,可促进许多下游信号转导,导致神经元死亡和脑组织损伤。此外,自噬是受损细胞器的再利用,在早期缺血时会受到影响。在缺血条件下,自噬在维持大脑能量及其功能方面发挥着重要作用。另一方面,细胞内 Ca2+ 过度积累会引发过度的自噬过程和溶酶体降解,导致自噬过程受损,最终诱发神经元死亡。本文综述了缺血性脑卒中急性期细胞内 Ca2+ 与自噬过程之间的关系。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
The underlying mechanism of calcium toxicity-induced autophagic cell death and lysosomal degradation in early stage of cerebral ischemia.

Cerebral ischemia is the important cause of worldwide disability and mortality, that is one of the obstruction of blood vessels supplying to the brain. In early stage, glutamate excitotoxicity and high level of intracellular calcium (Ca2+) are the major processes which can promote many downstream signaling involving in neuronal death and brain tissue damaging. Moreover, autophagy, the reusing of damaged cell organelles, is affected in early ischemia. Under ischemic conditions, autophagy plays an important role to maintain energy of the brain and its function. In the other hand, over intracellular Ca2+ accumulation triggers excessive autophagic process and lysosomal degradation leading to autophagic process impairment which finally induce neuronal death. This article reviews the association between intracellular Ca2+ and autophagic process in acute stage of ischemic stroke.

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来源期刊
Anatomy & Cell Biology
Anatomy & Cell Biology ANATOMY & MORPHOLOGY-
CiteScore
1.80
自引率
9.10%
发文量
75
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