肺动脉高压实验动物模型:发展与挑战。

Animal Models and Experimental Medicine Pub Date : 2022-09-01 Epub Date: 2022-03-25 DOI:10.1002/ame2.12220
Xiao-Han Wu, Jie-Ling Ma, Dong Ding, Yue-Jiao Ma, Yun-Peng Wei, Zhi-Cheng Jing
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引用次数: 10

摘要

肺动脉高压(Pulmonary hypertension, PH)在临床上分为5大类型,以肺动脉压(PAP)升高和肺血管阻力(PVR)为特征,最终导致右心衰而死亡。这种动脉病变的发病机制尚不清楚,因此不可能靶向肺血管重构并逆转右心室(RV)功能恶化。为了反映PH复杂的机制起源和病理,设计了不同的动物模型,根据建模方法大致分为4类:非侵入性体内模型、侵入性体内模型、基因编辑模型和多手段联合建模。虽然每种模型与不同类型的人类PH有一些共同的分子和病理变化,但在大多数情况下,人类PH的分子病因尚不清楚。适当使用经典和新颖的PH动物模型对于寻找分子靶标以逆转严重表型至关重要。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Experimental animal models of pulmonary hypertension: Development and challenges.

Experimental animal models of pulmonary hypertension: Development and challenges.

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.

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