Pulmonary hypertension: From molecular pathophysiology to haemodynamic abnormalities

被引:5
作者
Duong-Quy, S. [1 ]
Riviere, S. [1 ]
Bei, Y. [1 ]
Duong-Ngo, C. [1 ]
Le-Dong, N. N. [1 ]
Hua-Huy, T. [1 ]
Dinh-Xuan, A. T. [1 ]
机构
[1] Univ Paris 05, Serv Physiol, Hop Cochin, UPRES EA 2511,Fac Med, F-75104 Paris, France
关键词
Pulmonary hypertension; Pulmonary arterial hypertension; Physiopathology; Haemodynamic; Molecular pathology; VASOACTIVE-INTESTINAL-PEPTIDE; RHO-KINASE INHIBITOR; SMOOTH-MUSCLE-CELLS; 5-HYDROXYTRYPTAMINE TRANSPORTER GENE; SERINE ELASTASE INHIBITOR; CONGENITAL HEART-DISEASE; NITRIC-OXIDE SYNTHASE; ARTERIAL-HYPERTENSION; TENASCIN-C; TRANSGENIC MICE;
D O I
10.1016/j.rmr.2012.03.009
中图分类号
R56 [呼吸系及胸部疾病];
学科分类号
摘要
Pulmonary hypertension (PH) is a complex disorder resulting from many etiologies that cause disturbances of normal pulmonary haemodynamics. Recent breakthroughs have led to a better understanding of the pathophysiology of the disease. In PH, haemodynamic disturbances are closely linked to structural changes and excessive remodeling of pulmonary vessels, leading to progressive narrowing of the pulmonary vascular lumen. Imbalances between pulmonary vasoconstrictors and vasodilators on the one hand, and factors favoring cell proliferation and apoptosis on the other hand, probably account for most cases of PH. This review aims to update readers with the current knowledge on the molecular physiopathology of PH and how this can progress the therapeutic of this disorder. (C) 2012 SPLF. Published by Elsevier Masson SAS. All rights reserved.
引用
收藏
页码:956 / 970
页数:15
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