The potential role of TRPV1 in pulmonary hypertension: Angel or demon?

被引:10
|
作者
Zhang, Xin [1 ,2 ]
Ye, Lifang [2 ]
Huang, Yu [2 ]
Ding, Xueyan [2 ]
Wang, Lihong [1 ,2 ]
机构
[1] Zhejiang Chinese Med Univ, Clin Med Coll 2, Hangzhou, Zhejiang, Peoples R China
[2] Hangzhou Med Coll, Peoples Hosp, Zhejiang Prov Peoples Hosp, Dept Cardiovasc Med, Hangzhou, Zhejiang, Peoples R China
基金
中国国家自然科学基金;
关键词
Pulmonary hypertension; transient receptor potential vanilloid subfamily member 1; Ca2+; neuropeptides; inflammation; GENE-RELATED PEPTIDE; VANILLOID RECEPTOR SUBTYPE-1; NECROSIS-FACTOR-ALPHA; SMOOTH-MUSCLE-CELLS; ARTERIAL-HYPERTENSION; INFLAMMATORY RESPONSE; POSTISCHEMIC RECOVERY; EPITHELIAL-CELLS; SUBSTANCE-P; ACTIVATION;
D O I
10.1080/19336950.2019.1631106
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Pulmonary hypertension (PH) is a pathological state defined by increased pulmonary artery pressure, the pathogenesis of which is related to genetic mutations, intracellular calcium ([Ca2+](i)), inflammation and proliferation. Transient receptor potential vanilloid subfamily member 1 (TRPV1) is a nonselective cation channel expressed in neural and nonneural cells, including pulmonary vessels and nerves. As a calcium channel, TRPV1 can make vessels contracted, and promote smooth muscle cells proliferation through calcium-dependent transcription factors. Activation of TRPV1 in sensory nerves can release neuropeptides, including calcitonin gene-related peptide (CGRP), substance P (SP), and somatostatin (SST), which can regulate inflammation via transcription factor NF-kB. Considering the increased level of [Ca2+](i) and inflammation in the pathogenesis of PH, our review summarizes the role of TRPV1 in PH with regard to [Ca2+](i), neuropeptides, and inflammation. In view of the limited research illustrating the relationship between TRPV1 and PH directly, our review also considers the role of TRPV1 in other types of vascular inflammation. Through this review, we hope to raise awareness about the function of TRPV1 in PH.
引用
收藏
页码:235 / 246
页数:12
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