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细胞焦亡作为阿尔茨海默病的候选治疗靶点

Pyroptosis as a candidate therapeutic target for Alzheimer's disease.

作者信息

Huang Yuehua, Li Xiaoyu, Luo Guifei, Wang Junli, Li Ranhui, Zhou Chuyi, Wan Teng, Yang Fenglian

机构信息

Department of Reproductive Medicine, Affiliated Hospital of Youjiang Medical University for Nationalities, Baise, Guangxi, China.

Reproductive Medicine, Guangxi Medical and Health Key Discipline Construction Project of the Affiliated Hospital of Youjiang Medical University for Nationalities, Baise ,Guangxi, China.

出版信息

Front Aging Neurosci. 2022 Sep 15;14:996646. doi: 10.3389/fnagi.2022.996646. eCollection 2022.

DOI:10.3389/fnagi.2022.996646
PMID:36185484
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9520296/
Abstract

Pyroptosis is a form of cell death mediated by inflammasomes and gasdermins, and the relevance of pyroptosis to neurodegenerative diseases is currently receiving increasing attention. Alzheimer's disease (AD) is a chronic progressive neurodegenerative disease that is closely associated with neuroinflammation. Its main pathological features include β-amyloid (Aβ) deposition, Tau protein hyperphosphorylation and neuronal loss. Aβ, tau-induced microglia pyroptosis and polarization leading to neuroinflammation play an important role in the pathogenesis of AD. Studying the pathogenesis and treatment of AD based on cellular pyroptosis has become a new direction in AD research. In this paper, we review the research progress of pyroptosis and will focus on the pathogenic roles of pyroptosis in AD and the role of targeted inhibition of inflammasome-dependent pyroptosis in AD treatment. These results deepen our understanding of the pathogenesis of AD and provide ideas for the development of new drugs based on the regulation of pyroptosis in AD patients.

摘要

细胞焦亡是一种由炎性小体和gasdermin介导的细胞死亡形式,目前细胞焦亡与神经退行性疾病的相关性正受到越来越多的关注。阿尔茨海默病(AD)是一种慢性进行性神经退行性疾病,与神经炎症密切相关。其主要病理特征包括β-淀粉样蛋白(Aβ)沉积、Tau蛋白过度磷酸化和神经元丢失。Aβ、tau诱导的小胶质细胞焦亡和极化导致神经炎症,在AD的发病机制中起重要作用。基于细胞焦亡研究AD的发病机制和治疗方法已成为AD研究的一个新方向。本文综述了细胞焦亡的研究进展,并将重点关注细胞焦亡在AD中的致病作用以及靶向抑制炎性小体依赖性细胞焦亡在AD治疗中的作用。这些结果加深了我们对AD发病机制的理解,并为基于调节AD患者细胞焦亡开发新药提供了思路。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b04f/9520296/e64e51e7710b/fnagi-14-996646-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b04f/9520296/45fee2b4dfda/fnagi-14-996646-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b04f/9520296/e64e51e7710b/fnagi-14-996646-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b04f/9520296/45fee2b4dfda/fnagi-14-996646-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b04f/9520296/e64e51e7710b/fnagi-14-996646-g002.jpg

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