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Expression of ApoA5 and its function in the right ventricular failing and remodeling secondary to pulmonary hypertension
Author(s) -
Chen Jingyuan,
Luo Jun,
Yang Xiaojie,
Ouyang Minzhi,
Zhu Tengteng,
Li Yuanchang,
Luo Peng,
Chen Yusi,
Li Zilu,
Li Jiang
Publication year - 2021
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.29911
Subject(s) - pulmonary hypertension , extracellular matrix , medicine , fibroblast , fibrosis , heart failure , ventricular remodeling , cardiology , secretion , endocrinology , extracellular , cancer research , in vitro , microbiology and biotechnology , biology , biochemistry
Right heart failure and right ventricular (RV) remodeling were the main reason for mortality of pulmonary hypertension (PH) patients. Apolipoprotein AV (ApoA5) is a key regulator of plasma triglyceride and have multifunction in several target organs. We detected decreased ApoA5 in serum of patients with PH and both in serum and RV of monocrotaline‐induced PH model. Exogenously, overexpression ApoA5 by adenovirus showed protective effects on RV failure and RV fibrosis secondary to PH. In addition, in vitro experiments showed ApoA5 attenuated the activation of fibroblast induced by transforming growth factor β1 and synthesis and secretion of extracellular matrix by inhibiting focal adhesion kinase‐c‐Jun N‐terminal kinase‐Smad3 pathway. Finally, we suggest that ApoA5 may potentially be a pivotal target for RV failure and fibrosis secondary of PH.