{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nTRPM2 is an oxidant‐sensitive, Ca²⁺‐permeable, non‐selective cation channel that functions as a key sensor of cellular redox status. Activation of TRPM2 by reactive oxygen species and ADP‐ribose couples oxidative stress to Ca²⁺ influx, thereby modulating inflammatory signaling and promoting cell death in various immune cells such as macrophages and neutrophils. This channel has been implicated in inflammasome activation, cytokine production, and oxidative stress–mediated apoptotic pathways, ultimately influencing host defense and inflammatory pathologies. In several studies, TRPM2‐dependent Ca²⁺ entry has been shown to govern neutrophil cytotoxicity, microglial activation, and phagocyte function, underscoring its critical role as a molecular transducer of redox signals."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "12"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn the central nervous system, TRPM2 mediates diverse functions ranging from thermosensation and the regulation of body temperature to the modulation of synaptic plasticity, pain, and neuronal survival. TRPM2 channels expressed in hypothalamic and somatosensory neurons contribute to the perception of non‐noxious warmth and limit febrile responses, while in hippocampal neurons they influence long‐term depression and are implicated in excitotoxicity during ischemic insults. Moreover, regulation of neurite outgrowth and neural stem cell proliferation in response to thermal or oxidative stress has been linked to TRPM2 activity, which further impacts neuronal development and network connectivity."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "13", "end_ref": "24"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond the nervous system, TRPM2 plays pivotal roles in metabolic, cardiovascular, and hemostatic processes. In pancreatic β‐cells, TRPM2 activation is linked to Ca²⁺ influx that modulates insulin secretion and contributes to cell death under oxidative duress. In the cardiovascular system, TRPM2 activity influences myocardial responses to ischemia–reperfusion injury by regulating mitochondrial bioenergetics and ion homeostasis, while in hepatic cells, TRPM2 has been shown to mediate acetaminophen‐induced cytotoxicity. Additionally, TRPM2 is expressed in megakaryocytes where it participates in the regulation of platelet Ca²⁺ signaling, and modulation of the channel by Zn²⁺ or interacting proteins (such as EFHC1) further expands its impact on cell survival and even anti-tumor immunity through neutrophil-mediated mechanisms."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "25", "end_ref": "34"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Zhenyu Zhong, Yougang Zhai, Shuang Liang, et al. 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