Expression of ApoA5 and its function in the right ventricular failing and remodeling secondary to pulmonary hypertension
Expression of ApoA5 and its function in the right ventricular failing and remodeling secondary to pulmonary hypertension
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ApoA5在肺动脉高压继发右心室衰竭和重构中的表达及其作用
DOI：
10.1002/jcp.29911
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发表时间：
2020-06-30
影响因子：
5.6
通讯作者：
Li, Jiang
中科院分区：
文献类型：
--
作者：
Chen, Jingyuan;Luo, Jun;Li, Jiang
右心衰竭和右室重构是肺动脉高压（PH）患者死亡的主要原因。载脂蛋白AV（ApoA 5）是血浆甘油三酯的重要调节因子，在多个靶器官中具有多功能。我们检测到PH患者血清中以及野百合碱诱导的PH模型的血清和RV中的ApoA 5降低。外源性地，腺病毒过表达ApoA 5对PH继发的RV衰竭和RV纤维化显示出保护作用。此外，体外实验显示ApoA 5通过抑制黏着斑激酶-c-Jun N-末端激酶-Smad 3通路，减弱转化生长因子β1诱导的成纤维细胞活化和细胞外基质的合成和分泌。最后，我们认为ApoA 5可能是RV衰竭和继发于PH的纤维化的关键靶点。
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.