{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nTRPV3 is a non‐selective, Ca²⁺‐permeable ion channel of the transient receptor potential (TRP) family that is activated by warm temperatures in the physiological range and exhibits a unique use‐dependent sensitization with hysteretic gating. Initial investigations identified human TRPV3 in skin, tongue, dorsal root ganglia, and brain, where increasing temperature from approximately 22°C to 40°C leads to marked increases in intracellular Ca²⁺ via a steeply temperature‐dependent conductance. Unlike TRPV1, TRPV3 is insensitive to capsaicin but can function either alone or in combination with other TRP subunits, and its activity is profoundly modulated by intracellular factors such as ATP and calmodulin as well as specific binding phospholipids. Cryo‐electron microscopy studies have revealed dynamic rearrangements at the cytoplasmic inter–protomer interface that underlie its gating transitions and sensitization process, and biochemical studies demonstrate that intracellular Ca²⁺ regulation and ligand‐dependent shifts in voltage sensitivity contribute to its unique kinetic behavior."}, {"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 addition to its role as a thermosensor, TRPV3 is critically involved in modulating skin physiology and several pathophysiological processes. Gain‐of‐function mutations in TRPV3 have been causally linked to Olmsted syndrome, a congenital skin disorder marked by palmoplantar and periorificial keratoderma, alopecia, and severe pruritus; similar findings have highlighted its influence on keratinocyte proliferation, hair follicle differentiation, and the release of pro–inflammatory mediators. TRPV3 expression and activity have also been associated with abnormal inflammatory responses in atopic dermatitis, post–burn pruritus, and even oncogenic processes in non–small cell lung cancer. Beyond the skin, TRPV3 contributes to vascular function—for example, by generating Ca²⁺ “sparklets” that facilitate endothelium–dependent dilation of cerebral arterioles—as well as to sensory processes underlying migraine susceptibility and adipocyte differentiation. Moreover, studies have revealed that TRPV3 forms part of an intricate network where its regulation by endogenous ligands such as farnesyl pyrophosphate, its trafficking (including localization to lysosomes), and its genetic polymorphisms have potential therapeutic implications across a broad spectrum of disorders."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "13", "end_ref": "36"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Haoxing Xu, I Scott Ramsey, Suhas A Kotecha, et al. 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