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This study suggests that TRPV3 may play a key role in dry skin-related itch, indicating potential for TRPV3 antagonists in treating pruritus resistant to histamine H1R antagonists.

This review discusses the genetic causes and pathogenesis of Olmsted syndrome, emphasizing the potential for a genotype-phenotype correlation due to TRPV3 mutations, and explores avenues for individualized treatment developments for this condition.

This review discusses the expanding understanding of TRPV3's role in pain and skin pathology, while highlighting the need for further pharmacological research to fully resolve its functions.

TRPV4 slows hair growth by affecting hair follicle cells.

This review discusses current knowledge about the TRPV3 ion channel's role in skin functions and diseases, highlighting its potential as a therapeutic target for pain and itch, though suitable ligands are limited.

This laboratory study concluded that TRPA1 and TRPV1 channels do not play a role in mechanotransduction processes in slowly adapting type II mechanoreceptors in isolated rat sinus hair follicles.

This review explores the role of transient receptor potential vanilloid channels in the pathogenesis of osteoarthritis but reports no new clinical results.

This study found that Cannabidivarin (CBDV) promotes neuronal survival, proliferation, and differentiation via TRPV1 activation but inhibits oligodendrocyte differentiation in postnatal neurogenesis.

This study found that Cannabidivarin (CBDV) promotes neuronal differentiation and inhibits oligodendrocyte maturation via TRPV1 modulation, highlighting its potential in neural stem cell research.

This study found that activating TRPV4 in the skin of mice induced hair follicle regeneration by promoting anagen transition, suggesting potential treatment strategies for hair loss.

In this study, researchers explored various aspects of the TRPV3 ion channel, including its novel mechanosensitivity to shear stress, and identified novel agonists while investigating how repeated stimulation affects TRPV3 activity, but found no evidence of GPCRs sensitizing the channel.

This study found that activation of the TRPV3 ion channel inhibits human hair growth by affecting hair follicles and outer root sheath keratinocytes.

This study found that TRPV3 ion channels on human epidermal keratinocytes suppress cell proliferation, induce cell death, and trigger a proinflammatory response, suggesting a role in cutaneous inflammatory processes.

This review examined the role of the ion channel TRPV3 in warmth sensation and skin physiology, discussing controversies around its direct contribution to temperature perception, its involvement in skin health, and its potential as a therapeutic target for skin diseases.

In this study, researchers used cryo-electron microscopy to reveal how the natural compound osthole inhibits TRPV3 channels by binding to specific sites, changing the channel's conformation.

This study found that TRPV3 activation in human sebocytes inhibits lipid synthesis and triggers proinflammatory cytokine expression, suggesting a role in the pathogenesis of dry skin-associated inflammatory dermatoses.

This study found that activating CB1 receptor signaling in human hair follicles increased stem cell proliferation while reducing differentiated cell survival, suggesting CB1's role as a survival stimulus for epithelial stem cells.

This review article addresses how the TRPV4 ion channel helps cells respond to mechanical and environmental stimuli, discussing its role in calcium signaling crucial for tissue repair and fibrosis across various organ systems, and highlighting potential therapeutic targets from animal and disease models.

This study found that inhibiting the TRPV3 channel may significantly promote hair growth and suggests a potential therapeutic approach for hair loss and related skin diseases.

In this study, activating TRPV1 nociceptors in mice skin stimulated dormant hair follicles and promoted hair growth through a mechanism involving dermal macrophages, fibroblasts, and neuropeptides, highlighting a new role for nociceptors in tissue recovery after injury.

In this study, calcium imaging in transgenic mice revealed that non-neuronal TRPV4 in the skin enhances afferent signaling during electrical stimulation, suggesting a role for neuroimmune interaction in acupuncture signal initiation.

Sensitive skin is often caused by nerve fibers and environmental factors, and can be managed with mild skincare and professional advice.

This review discusses lung regeneration and highlights the role of facultative stem/progenitor cells, but it reports no new findings and calls for further exploration of underlying mechanisms.

This review discusses the regulation of hair growth, causes of excessive androgen secretion, and current safe solutions for hyperandrogenism manifestations in women but reports no new clinical results.

This study found that TRPV1 activation in human scalp hair follicles inhibited hair shaft elongation, suppressed proliferation, and induced apoptosis, suggesting TRPV1 as a potential target for managing hair growth and epithelial disorders.

In this study, mouse sweat gland development relied on a regulatory sequence initiated by Wnt/β-catenin signaling, and disruptions in Wnt, Eda, or Shh pathways led to distinct developmental failures.

In this study, DHT was found to inhibit hair growth in mice by decreasing IGF-I production in dermal papillae through reduced sensory neuron stimulation.

This study observed that in an ex vivo setting, 17β-estradiol increased CB1 expression in human hair follicles, suggesting possible sensitivity to endocannabinoids and a potential mechanism for hair therapy.

This study found that specific TRPM5 modulators are unlikely to directly affect sebaceous glands, but safe TPPO analogues may provide moderate lipogenic and anti-inflammatory effects beneficial for dry skin conditions.

This study found a 93.5% increase in nonvellus hair after 6 months of daily topical CBD application on the scalp in individuals with androgenetic alopecia, with no reported adverse effects.