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Research on the Regulatory Role of MAMs in NLRP3 Inflammasome in Ischemic Stroke

SU Gengzheng^1#, DONG Yuanyuan^2#, XU Jiahao², LI Chenxiao¹, WANG Yue³, ZHANG Shuang³, WANG Yanping⁴, WANG Ke²*, HE Zhi2*

（¹College of Life Sciences and Medicine, Zhejiang Sci-Tech University, Hangzhou 310018, China; ²College of Medicine, Jiaxing University, Jiaxing 314001, China; ²College of Medicine and Health Sciences, China Three Gorges University, Yichang 443002, China; ⁴Department of Neurology, the Second Affiliated Hospital of Jiaxing University, Jiaxing 314000, China)

Abstract:

IS (ischemic stroke) is one of the leading causes of death in humans, characterized by high inci dence, mortality, and recurrence rates. Following IS, the activation of the NLRP3 inflammasome and the release of IL-1β (interleukin-1β) and IL-18 mediate the inflammatory response following the stroke. MAMs (mitochondria associated endoplasmic reticulum membranes) are specialized structures formed by the physical contact between mitochondria and the endoplasmic reticulum, and they are widely involved in processes such as the generation of ROS (reactive oxygen species), ERS (endoplasmic reticulum stress), mitophagy, and Ca2+ homeostasis. These pro cesses are closely related to the NLRP3-mediated inflammatory response. This article focuses on the role of MAMs in IS, with the NLRP3 inflammasome as the central theme. The NLRP3 inflammasome and MAMs may represent potential therapeutic targets for treating IS, offering new research insights for the treatment of ischemic brain injury.

CSTR: 32200.14.cjcb.2025.11.0024