Autophapy-NLRP3 Inflammasome Crosstalk в Микроглии: терапевтическая цель для множественного склероза.
Обработка статьи · этапы, ошибки и управление
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Lu Jie-Qiong, Wang Hui-Qi, Fang Ma-Rong, Ye Xiang-Ming, Song Kai-Yi
Аннотация
Оригинал публикации
Autophagy-NLRP3 Inflammasome Crosstalk in Microglia: A Therapeutic Target for Multiple Sclerosis.
Multiple sclerosis (MS) affects approximately 2.9 million people globally, and targeting the nod-like receptor protein 3 (NLRP3) inflammasome and microglial autophagy is critical for preventing disease development. Microglia contribute to the onset and progression of MS by maintaining inflammatory reactions and removing cellular debris. Autophagy can maintain cellular homeostasis and alleviate inflammatory responses in the central nervous system (CNS). Autophagy is an important mechanism of cellular degradation and circulation that helps maintain cellular homeostasis and alleviate inflammatory responses. The NLRP3 inflammasome is an important component of the innate immune system. It recognizes additional invasions and internal stimuli, triggering an inflammatory response of neuroinflammation. The neuroinflammatory systems and features of MS are reviewed here. We focused on the functional regulation and polarization of microglia. We also examined how autophagy and the NLRP3 inflammasome interact and their underlying biological mechanisms. Moreover, on the basis of existing research, we explored the potential of relevant biomarkers for MS diagnosis and treatment and examined possible therapeutic strategies targeting the autophagy-NLRP3 inflammasome axis. Furthermore, we summarize recent research on the efficacy of drugs targeting the autophagy-NLRP3 inflammasome pathway in reducing neuroinflammation and alleviating MS while addressing potential challenges associated with pharmacological interventions for MS.