TRPV3 and Itch: The Role of TRPV3 in Chronic Pruritus according to Clinical and Experimental Evidence
Itching is a sensory phenomenon characterized by an unpleasant sensation that makes you want to scratch the skin, and chronic itching diminishes the quality of life. In recent studies, multiple transient receptor potential (TRP) channels present in keratinocytes or nerve endings have been shown to e...
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MDPI AG
2022-11-01
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author | Ji Young Um Han Bi Kim Jin Cheol Kim Jin Seo Park So Yeon Lee Bo Young Chung Chun Wook Park Hye One Kim |
author_facet | Ji Young Um Han Bi Kim Jin Cheol Kim Jin Seo Park So Yeon Lee Bo Young Chung Chun Wook Park Hye One Kim |
author_sort | Ji Young Um |
collection | DOAJ |
description | Itching is a sensory phenomenon characterized by an unpleasant sensation that makes you want to scratch the skin, and chronic itching diminishes the quality of life. In recent studies, multiple transient receptor potential (TRP) channels present in keratinocytes or nerve endings have been shown to engage in the propagation of itch signals in chronic dermatological or pruritic conditions, such as atopic dermatitis (AD) and psoriasis (PS). TRPV3, a member of the TRP family, is highly expressed in the epidermal keratinocytes. Normal TRPV3 signaling is essential for maintaining epidermal barrier homeostasis. In recent decades, many studies have suggested that TRPV3 contributes to detecting pruritus signals. Gain-of-function mutations in TRPV3 in mice and humans are characterized by severe itching, hyperkeratosis, and elevated total IgE levels. These studies suggest that TRPV3 is an important channel for skin itching. Preclinical studies have provided evidence to support the development of TRPV3 antagonists for treating inflammatory skin conditions, itchiness, and pain. This review explores the role of TRPV3 in chronic pruritus, collating clinical and experimental evidence. We also discuss underlying cellular and molecular mechanisms and explore the potential of TRPV3 antagonists as therapeutic agents. |
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language | English |
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spelling | doaj.art-10f982921fee4772a6acdf5ce2204b762023-11-24T11:10:51ZengMDPI AGInternational Journal of Molecular Sciences1661-65961422-00672022-11-0123231496210.3390/ijms232314962TRPV3 and Itch: The Role of TRPV3 in Chronic Pruritus according to Clinical and Experimental EvidenceJi Young Um0Han Bi Kim1Jin Cheol Kim2Jin Seo Park3So Yeon Lee4Bo Young Chung5Chun Wook Park6Hye One Kim7Department of Dermatology, College of Medicine, Hallym University Kangnam Sacred Heart Hospital, Seoul 150-950, Republic of KoreaDepartment of Dermatology, College of Medicine, Hallym University Kangnam Sacred Heart Hospital, Seoul 150-950, Republic of KoreaDepartment of Dermatology, College of Medicine, Hallym University Kangnam Sacred Heart Hospital, Seoul 150-950, Republic of KoreaDepartment of Dermatology, College of Medicine, Hallym University Kangnam Sacred Heart Hospital, Seoul 150-950, Republic of KoreaDepartment of Dermatology, College of Medicine, Hallym University Kangnam Sacred Heart Hospital, Seoul 150-950, Republic of KoreaDepartment of Dermatology, College of Medicine, Hallym University Kangnam Sacred Heart Hospital, Seoul 150-950, Republic of KoreaDepartment of Dermatology, College of Medicine, Hallym University Kangnam Sacred Heart Hospital, Seoul 150-950, Republic of KoreaDepartment of Dermatology, College of Medicine, Hallym University Kangnam Sacred Heart Hospital, Seoul 150-950, Republic of KoreaItching is a sensory phenomenon characterized by an unpleasant sensation that makes you want to scratch the skin, and chronic itching diminishes the quality of life. In recent studies, multiple transient receptor potential (TRP) channels present in keratinocytes or nerve endings have been shown to engage in the propagation of itch signals in chronic dermatological or pruritic conditions, such as atopic dermatitis (AD) and psoriasis (PS). TRPV3, a member of the TRP family, is highly expressed in the epidermal keratinocytes. Normal TRPV3 signaling is essential for maintaining epidermal barrier homeostasis. In recent decades, many studies have suggested that TRPV3 contributes to detecting pruritus signals. Gain-of-function mutations in TRPV3 in mice and humans are characterized by severe itching, hyperkeratosis, and elevated total IgE levels. These studies suggest that TRPV3 is an important channel for skin itching. Preclinical studies have provided evidence to support the development of TRPV3 antagonists for treating inflammatory skin conditions, itchiness, and pain. This review explores the role of TRPV3 in chronic pruritus, collating clinical and experimental evidence. We also discuss underlying cellular and molecular mechanisms and explore the potential of TRPV3 antagonists as therapeutic agents.https://www.mdpi.com/1422-0067/23/23/14962transient receptor potential vanilloid-3chronic pruritusitchingatopic dermatitispsoriasis |
spellingShingle | Ji Young Um Han Bi Kim Jin Cheol Kim Jin Seo Park So Yeon Lee Bo Young Chung Chun Wook Park Hye One Kim TRPV3 and Itch: The Role of TRPV3 in Chronic Pruritus according to Clinical and Experimental Evidence International Journal of Molecular Sciences transient receptor potential vanilloid-3 chronic pruritus itching atopic dermatitis psoriasis |
title | TRPV3 and Itch: The Role of TRPV3 in Chronic Pruritus according to Clinical and Experimental Evidence |
title_full | TRPV3 and Itch: The Role of TRPV3 in Chronic Pruritus according to Clinical and Experimental Evidence |
title_fullStr | TRPV3 and Itch: The Role of TRPV3 in Chronic Pruritus according to Clinical and Experimental Evidence |
title_full_unstemmed | TRPV3 and Itch: The Role of TRPV3 in Chronic Pruritus according to Clinical and Experimental Evidence |
title_short | TRPV3 and Itch: The Role of TRPV3 in Chronic Pruritus according to Clinical and Experimental Evidence |
title_sort | trpv3 and itch the role of trpv3 in chronic pruritus according to clinical and experimental evidence |
topic | transient receptor potential vanilloid-3 chronic pruritus itching atopic dermatitis psoriasis |
url | https://www.mdpi.com/1422-0067/23/23/14962 |
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