Gao Yahao, Wang Changshui, Jiang Di, An Gang, Jin Feng, Zhang Junchen, Han Guangkui, Cui Changmeng, Jiang Pei
Clinical Medical School, Jining Medical University, Jining, China.
Department of Neurosurgery, Affiliated Hospital of Jining Medical University, Jining, China.
Front Cell Dev Biol. 2022 Sep 16;10:994037. doi: 10.3389/fcell.2022.994037. eCollection 2022.
Autophagy is a dynamic process that maintains the normal homeostasis of cells by digesting and degrading aging proteins and damaged organelles. The effect of autophagy on neural tissue is still a matter of debate. Some authors suggest that autophagy has a protective effect on nerve cells, whereas others suggest that autophagy also induces the death of nerve cells and aggravates nerve injury. In mammals, oxidative stress, autophagy and endoplasmic reticulum stress (ERS) constitute important defense mechanisms to help cells adapt to and survive the stress conditions caused by physiological and pathological stimuli. Under many pathophysiological conditions, oxidative stress, autophagy and ERS are integrated and amplified in cells to promote the progress of diseases. Over the past few decades, oxidative stress, autophagy and ERS and their interactions have been a hot topic in biomedical research. In this review, we summarize recent advances in understanding the interactions between oxidative stress, autophagy and ERS in neuronal cell death and survival.
自噬是一个动态过程,通过消化和降解衰老蛋白质及受损细胞器来维持细胞的正常稳态。自噬对神经组织的影响仍存在争议。一些作者认为自噬对神经细胞具有保护作用,而另一些人则认为自噬也会诱导神经细胞死亡并加重神经损伤。在哺乳动物中,氧化应激、自噬和内质网应激(ERS)构成重要的防御机制,以帮助细胞适应并在生理和病理刺激引起的应激条件下存活。在许多病理生理条件下,氧化应激、自噬和ERS在细胞中相互整合并放大,以促进疾病进展。在过去几十年中,氧化应激、自噬和ERS及其相互作用一直是生物医学研究的热点话题。在这篇综述中,我们总结了在理解氧化应激、自噬和ERS在神经元细胞死亡和存活中的相互作用方面的最新进展。