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肺动脉高压的实验动物模型:建立与挑战。

Experimental animal models of pulmonary hypertension: Development and challenges.

机构信息

Department of Cardiology, State Key Laboratory of Complex Severe and Rare Diseases, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.

Medical Science Research Center, State Key Laboratory of Complex Severe and Rare Diseases, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.

出版信息

Animal Model Exp Med. 2022 Sep;5(3):207-216. doi: 10.1002/ame2.12220. Epub 2022 Mar 25.

Abstract

Pulmonary hypertension (PH) is clinically divided into 5 major types, characterized by elevation in pulmonary arterial pressure (PAP) and pulmonary vascular resistance (PVR), finally leading to right heart failure and death. The pathogenesis of this arteriopathy remains unclear, leaving it impossible to target pulmonary vascular remodeling and reverse the deterioration of right ventricular (RV) function. Different animal models have been designed to reflect the complex mechanistic origins and pathology of PH, roughly divided into 4 categories according to the modeling methods: non-invasive models in vivo, invasive models in vivo, gene editing models, and multi-means joint modeling. Though each model shares some molecular and pathological changes with different classes of human PH, in most cases the molecular etiology of human PH is poorly known. The appropriate use of classic and novel PH animal models is essential for the hunt of molecular targets to reverse severe phenotypes.

摘要

肺动脉高压(PH)临床上分为 5 大类型,其特征是肺动脉压(PAP)和肺血管阻力(PVR)升高,最终导致右心衰竭和死亡。这种血管疾病的发病机制尚不清楚,无法靶向肺血管重塑和逆转右心室(RV)功能的恶化。已经设计了不同的动物模型来反映 PH 的复杂机制起源和病理学,大致根据建模方法分为 4 类:体内非侵入性模型、体内侵入性模型、基因编辑模型和多种方法联合建模。尽管每种模型都与不同类型的人类 PH 存在一些分子和病理变化,但在大多数情况下,人类 PH 的分子病因尚不清楚。适当使用经典和新型 PH 动物模型对于寻找逆转严重表型的分子靶标至关重要。

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