{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nTRPV3 is a warm‐activated, Ca²⁺‐permeable cation channel that is predominantly expressed in skin keratinocytes and several other epithelia. Multiple studies have shown that TRPV3 plays a central role in thermosensation, mediating responses to innocuous warmth as well as noxious heat. Its activation in keratinocytes triggers the release of diffusible mediators (such as ATP, nitric oxide, and prostaglandin E₂) that in turn signal to neighboring sensory nerve terminals, thereby contributing to both heat detection and nociception. Moreover, TRPV3 interacts with key growth factor pathways such as TGF‐α/EGFR that regulate keratinocyte proliferation, skin barrier formation, and hair morphogenesis. These mechanisms provide the basis for understanding how TRPV3 activation underpins thermosensory perception and contributes to cutaneous functions."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "10"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn addition to its role in thermosensory signaling, aberrant TRPV3 activity has been linked to pathological phenotypes. Gain‐of‐function mutations in TRPV3 lead to constitutive channel activation that causes spontaneous dermatitis, pruritus, and hair loss in rodent models. Structural studies have revealed that TRPV3 undergoes distinct conformational transitions—from α‐helical to π‐helical arrangements in the S6 segment—and that these changes, along with lipid interactions, contribute to its gating. The channel’s sensitivity is further modulated by intracellular Ca²⁺ and calmodulin, as well as by naturally occurring compounds (e.g., camphor, osthole, and (-)-epicatechin), which can either enhance or inhibit its activity. These diverse regulatory mechanisms underscore the contribution of TRPV3 not only to normal skin homeostasis but also to inflammatory skin disorders and abnormal sensory processing."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "11", "end_ref": "20"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond its functions in the skin, TRPV3 also contributes to physiological responses in other tissues, such as the gastrointestinal tract, where it modulates epithelial calcium responses and ATP release. In vivo studies have demonstrated that TRPV3-mediated signaling not only influences local vasodilation through the release of calcitonin gene-related peptide and nitric oxide but also cooperates with TRPV1 to define the threshold for moderate and noxious heat perception. This repertoire of functions positions TRPV3 as an attractive therapeutic target for treating pruritic and inflammatory conditions, pain, and even metabolic dysregulations. Moreover, modulation of TRPV3 by natural small molecules continues to offer promising strategies for pharmacological intervention."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "21", "end_ref": "32"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Andrea M Peier, Alison J Reeve, David A Andersson, et al. 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