Emerging Role of Transient Receptor Potential Vanilloid 4 (TRPV4) Ion Channel in Acute and Chronic Itch.
Emerging Role of Transient Receptor Potential Vanilloid 4 (TRPV4) Ion Channel in Acute and Chronic Itch.
复制标题
DOI：
10.3390/ijms22147591
复制
发表时间：
2021-07-15
影响因子：
5.6
通讯作者：
Chen Y
中科院分区：
文献类型：
--
作者：
Zhang Q;Henry G;Chen Y
瘙痒是一种临床问题，导致许多患者得不到充分治疗，在美国有超过2000万例。这是由于对其分子、细胞和细胞间信号传导机制的不完全理解。瞬时受体电位（TRP）离子通道参与多种感觉形式，包括疼痛、视觉、味觉、嗅觉、听觉、触觉和温度感觉以及瘙痒。相对于对TRPV1和TRPA1离子通道在瘙痒调节中的广泛研究，TRPV4受到的研究关注相对较少，直到最近，对其机制仍然知之甚少。TRPV4在神经节感觉神经元和多种皮肤细胞中表达。过去几年越来越多的证据强烈表明，这些细胞中的TRPV4有助于急性和慢性疾病相关的瘙痒。本文就TRPV4在瘙痒病理生理过程中的作用及其可能的细胞和分子机制进行综述。
Itch is a clinical problem that leaves many sufferers insufficiently treated, with over 20 million cases in the United States. This is due to incomplete understanding of its molecular, cellular, and cell-to-cell signaling mechanisms. Transient receptor potential (TRP) ion channels are involved in several sensory modalities including pain, vision, taste, olfaction, hearing, touch, and thermosensation, as well as itch. Relative to the extensive studies on TRPV1 and TRPA1 ion channels in itch modulation, TRPV4 has received relatively little research attention and its mechanisms have remained poorly understood until recently. TRPV4 is expressed in ganglion sensory neurons and a variety of skin cells. Growing evidence in the past few years strongly suggests that TRPV4 in these cells contributes to acute and chronic disease-associated itch. This review focuses on the current experimental evidence involving TRPV4 in itch under pathophysiological conditions and discusses its possible cellular and molecular mechanisms.
登录
查看更多内容
影响因子：
2.6
作者：
Kostner, Lisa;Anzengruber, Florian;Navarini, Alexander A.
通讯作者：
Navarini, Alexander A.
影响因子：
2.7
作者：
Kanju P;Liedtke W
通讯作者：
Liedtke W
影响因子：
7.4
作者：
Chen Y;Williams SH;McNulty AL;Hong JH;Lee SH;Rothfusz NE;Parekh PK;Moore C;Gereau RW 4th;Taylor AB;Wang F;Guilak F;Liedtke W
通讯作者：
Liedtke W
影响因子：
--
作者：
Dull, Miriam M;Kremer, Andreas E
通讯作者：
Kremer, Andreas E
影响因子：
2.7
作者：
Akazawa, Y.;Yuki, T.;Inoue, S.
通讯作者：
Inoue, S.