Fetal Gene Reactivation in Pulmonary Arterial Hypertension: GOOD, BAD, or BOTH?

被引：9

作者：

Lemay, Sarah-Eve ^{[1
]}

Awada, Charifa ^{[1
]}

Shimauchi, Tsukasa ^{[1
]}

Wu, Wen-Hui ^{[1
,2
]}

Bonnet, Sebastien ^{[1
]}

Provencher, Steeve ^{[1
]}

Boucherat, Olivier ^{[1
]}

机构：

[1] Inst Univ Cardiol & Pneumol Quebec, Pulm Hypertens Res Grp, Ctr Rech, Quebec City, PQ G1V 4G5, Canada

[2] Tongji Univ, Shanghai Pulm Hosp, Dept Cardio Pulm Circulat, Sch Med, Shanghai 200433, Peoples R China

来源：

CELLS | 2021年 / 10卷 / 06期

关键词：

vascular remodeling; cardiac hypertrophy; right ventricular failure; development; MUSCLE-CELL-PROLIFERATION; CARDIAC-HYPERTROPHY; RIGHT VENTRICLE; TRANSCRIPTION FACTOR; MICE LACKING; TENASCIN-C; PHARMACOLOGICAL INHIBITION; ACETYLTRANSFERASE ACTIVITY; MYOCARDIAL-CONTRACTILITY; CALCINEURIN INHIBITORS;

D O I：

10.3390/cells10061473

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

Pulmonary arterial hypertension is a debilitating chronic disorder marked by the progressive obliteration of the pre-capillary arterioles. This imposes a pressure overload on the right ventricle (RV) pushing the latter to undergo structural and mechanical adaptations that inexorably culminate in RV failure and death. Thanks to the advances in molecular biology, it has been proposed that some aspects of the RV and pulmonary vascular remodeling processes are orchestrated by a subversion of developmental regulatory mechanisms with an upregulation of a suite of genes responsible for the embryo's early growth and normally repressed in adults. In this review, we present relevant background regarding the close relationship between overactivation of fetal genes and cardiopulmonary remodeling, exploring whether the reawakening of developmental factors plays a causative role or constitutes a protective mechanism in the setting of PAH.

引用

页数：19

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