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作 者:Xiao-Han Wu Jie-Ling Ma Dong Ding Yue-Jiao Ma Yun-Peng Wei Zhi-Cheng Jing
机构地区:[1]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 [2]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 处:《Animal Models and Experimental Medicine》2022年第3期207-216,共10页动物模型与实验医学(英文)
基 金:CAMS Innovation Fund for Medical Sciences (CIFMS):2021-I2M-1-018。
摘 要: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: noninvasive 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.
关 键 词:animal models BMPR2 chronic hypoxia MONOCROTALINE pulmonary hypertension Sugen 5416
分 类 号:R544.1[医药卫生—心血管疾病] R-332[医药卫生—内科学]
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