Expression of ApoA5 and its function in the right ventricular failing and remodeling secondary to pulmonary hypertension. Issue 2 (30th June 2020)

• Record Type: Journal Article
• Authors: Chen, Jingyuan; Luo, Jun; Yang, Xiaojie; Ouyang, Minzhi; Zhu, Tengteng; Li, Yuanchang; Luo, Peng; Chen, Yusi; Li, Zilu; Li, Jiang
• Is Part Of: Journal of cellular physiology. Volume 236:Issue 2(2021)
• Page Start: 1013
• Page End: 1024
• Publication Date: 2020-06-30
• Subjects: apolipoprotein A5 -- right heart failure -- right ventricular fibrosis; Physiology -- Periodicals; Cell physiology -- Periodicals; 571.6
• DOI: 10.1002/jcp.29911
• Languages: English
• ISSNs: 0021-9541

Abstract

Abstract: 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. Abstract : Apolipoprotein AV (ApoA5) was decreased in patients with pulmonary hypertension (PH) as well as a monocrotaline‐induced PH model. Overexpression ApoA5 can help protect from the right ventricular failing and remodeling secondary to pulmonary hypertension.