TRPs modulate inflammation in immune cells

TRPs modulate inflammation in immune cells. The activation of TRPC6, TRPC3, TRPV4, and TRPM2 leads to Ca2+ influx, which then triggers the AKT/MAPK signaling pathway to enhance the expression of pro-inflammatory genes. When TRPC1 or TRPC3 is activated, it allows for increased calcium influx and subsequently activates the phosphorylation of JNK/STAT1 or STAT6, or JAK/STAT3, respectively, to promote the release of pro-inflammatory factors. Stimulation of TRPC3 induces pro-inflammatory gene expression via PKC signaling. Activation of the TRPV1 channel results in calcium entry and subsequent activation of PP2A to activate the NLRP3 inflammasome, thereby promoting an inflammatory response. When Ca2+ ions flow out of the lysosome via the TRPM2 ion channel, it leads to an increase in intracellular calcium concentration, which further activates the MAPK pathway. Inhibition of NADPH oxidase activity can enhance the production of reactive oxygen species (ROS) and activate the MAPK pathway, resulting in the phosphorylation of NF-κB and its translocation into the nucleus, thereby leading to the production of pro-inflammatory factors. Activation of TRPM4 and TRPM5 channels can induce sodium influx and trigger NLRP3 inflammasome activation, thus contributing to inflammation. Activation of TRPM7 triggers signaling pathways such as AKT/mTOR, STAT5-Foxp3, or Ca2+/CaMKII/TRAF6, leading to pro-inflammatory gene transcription

Publication

TRP Ion Channels in Immune Cells and Their Implications for Inflammation (2024) Qiyue Yan, et al. Int J Mol Sci. 2024 Mar;25(5). Figure: F1. Homo sapiens

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