Serotonin and pulmonary hypertension-from bench to bedside?

被引：74

作者：

MacLean, Margaret R. ^{[1
]}

Dempsie, Yvonne ^{[1
]}

机构：

[1] Univ Glasgow, Fac Biomed & Life Sci, Glasgow G12 8QQ, Lanark, Scotland

来源：

CURRENT OPINION IN PHARMACOLOGY | 2009年 / 9卷 / 03期

基金：

英国生物技术与生命科学研究理事会;

关键词：

SMOOTH-MUSCLE-CELLS; 5-HYDROXYTRYPTAMINE TRANSPORTER GENE; MEDIATED VASOCONSTRICTION; CONVERGING EVIDENCE; GERMLINE MUTATIONS; RECEPTOR; DEXFENFLURAMINE; FENFLURAMINE; BMPR2; HYPERPLASIA;

D O I：

10.1016/j.coph.2009.02.005

中图分类号：

R9 [药学];

学科分类号：

1007 ;

摘要：

The serotonin hypothesis of pulmonary arterial hypertension (PAH) arose owing to anorexigens, acting as indirect serotinergic agonists, causing PAH. However, it is now thought that serotonin plays an important role in the pathobiology of PAH per se. The rate-limiting enzyme in the synthesis of peripheral serotonin is tryptophan hydroxylase 1 (TPH1), serotonin can mediate pulmonary arterial smooth muscle cell proliferation via the serotonin transporter (SERT) and serotonin can induce pulmonary vasoconstriction via the 5-HT1B receptor in man. There is evidence that TPH1, SERT and 5-HT1B expression/activity can be upregulated in clinical PAH. This review discusses recent evidence implicating serotonin in the development of experimental and clinical PAH and suggests potential therapeutic targets.

引用

页码：281 / 286

页数：6

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