TRPM2

TRPM2 is a Ca2+-permeable, non-selective cation channel activated by temperature, oxidative stress, and NAD+-related metabolites such as ADP-ribose[1]. Mechanistically, TRPM2 connects reactive oxygen species to Ca2+ influx, immune response, apoptosis, and core body temperature regulation[1]. In inflammatory models, TRPM2-mediated Ca2+ influx drives chemokine production in monocytes and aggravates neutrophil infiltration[2]. TRPM2 also links oxidative stress to NLRP3 inflammasome activation, and Trpm2−/− mice resist crystal- or liposome-induced IL-1β-mediated peritonitis[3]. In sensory physiology, TRPM2 is required for non-noxious warmth detection in mice, defining a heat-sensitive role distinct from cold- and menthol-activated TRPM8[4]. For experimental applications, 2-APB rapidly and reversibly inhibits ADP-ribose-, cADPR-, and heat-activated TRPM2, while ACA inhibits H2O2-induced TRPM2-mediated Ca2+ entry in β-cells[5][6].