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Expression of ApoA5 and its function in the right ventricular failing and remodeling secondary to pulmonary hypertension.
Journal of Cellular Physiology ( IF 4.5 ) Pub Date : 2020-06-30 , DOI: 10.1002/jcp.29911
Jingyuan Chen 1 , Jun Luo 1 , Xiaojie Yang 1 , Minzhi Ouyang 1, 2 , Tengteng Zhu 1 , Yuanchang Li 1 , Peng Luo 1 , Yusi Chen 1 , Zilu Li 1 , Jiang Li 1
Affiliation  

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.

中文翻译:

ApoA5的表达及其在肺动脉高压继发右心室衰竭和重构中的作用。

右心衰竭和右心室(RV)重构是肺动脉高压(PH)患者死亡的主要原因。载脂蛋白 AV (ApoA5) 是血浆甘油三酯的关键调节因子,在多个靶器官中具有多种功能。我们检测到 PH 患者血清以及野百合碱诱导的 PH 模型的血清和 RV 中的 ApoA5 降低。外源性地,腺病毒过表达 ApoA5 对 RV 衰竭和继发于 PH 的 RV 纤维化显示出保护作用。此外,体外实验表明,ApoA5通过抑制粘着斑激酶-c-Jun N-末端激酶-Smad3通路,减弱了转化生长因子β1诱导的成纤维细胞的活化和细胞外基质的合成和分泌。最后,我们建议 ApoA5 可能是 RV 衰竭和 PH 继发纤维化的关键目标。
更新日期:2020-06-30
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