The Roles of FGF21 and ALCAT1 in Aerobic Exercise-Induced Cardioprotection of Postmyocardial Infarction Mice.
The Roles of FGF21 and ALCAT1 in Aerobic Exercise-Induced Cardioprotection of Postmyocardial Infarction Mice.
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FGF21和ALCAT1在有氧运动诱导的心肌梗死后小鼠心脏保护中的作用
DOI：
10.1155/2021/8996482
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发表时间：
2021
影响因子：
--
通讯作者：
Tian Z
中科院分区：
文献类型：
--
作者：
Bo W;Ma Y;Xi Y;Liang Q;Cai M;Tian Z
有氧运动减轻心肌梗死（MI）引起的氧化应激和细胞凋亡，尽管确切的机制仍然完全不清楚。本研究旨在探讨有氧运动改善心肌梗死小鼠心功能的可能机制。在体内，MI诱导左前降支（LAD）冠状动脉结扎野生型小鼠，alcat 1基因敲除，和fgf 21基因敲除小鼠。在MI后一周，小鼠在中等强度方案下运动6周。在体外，用携带alcat 1基因的慢病毒载体、重组人FGF 21（rhFGF 21）、PI 3 K抑制剂和H2 O2处理H9 C2细胞，以探讨其可能的机制。我们的研究结果表明，有氧运动显着增加心肌梗死小鼠心脏中的FGF 21的表达和ALCAT 1的表达下降。fgf 21基因敲除减弱了有氧运动对MI小鼠氧化应激、内质网应激和细胞凋亡的抑制作用。alcat 1基因敲除和/或有氧运动通过抑制MI心脏的氧化应激和细胞凋亡来改善心脏功能。rhFGF 21通过激活H9 C2细胞中的PI 3 K/AKT通路抑制H2 O2和ALCAT 1诱导的氧化应激和凋亡的过表达。结论：有氧运动可通过激活FGF 21/FGFR 1/PI 3 K/AKT通路或抑制ALCAT 1的过度表达，减轻氧化应激和细胞凋亡，从而改善MI小鼠的心功能。
Aerobic exercise mitigates oxidative stress and apoptosis caused by myocardial infarction (MI) even though the precise mechanisms remain completely elusive. In this study, we investigated the potential mechanisms of aerobic exercise in ameliorating the cardiac function of mice with MI. In vivo, MI was induced by left anterior descending (LAD) coronary artery ligation in wild-type mice, alcat1 knockout, and fgf21 knockout mice. The mice were exercised under a moderate-intensity protocol for 6 weeks at one week later post-MI. In vitro, H9C2 cells were treated with lentiviral vector carrying alcat1 gene, recombinant human FGF21 (rhFGF21), PI3K inhibitor, and H2O2 to explore the potential mechanisms. Our results showed that aerobic exercise significantly increased the FGF21 expression and decreased the ALCAT1 expression in the hearts of mice with MI. fgf21 knockout weakened the inhibitory effects of aerobic exercise on oxidative stress, endoplasmic reticulum (ER) stress, and apoptosis in mice with MI. Both/either alcat1 knockout and/or aerobic exercise improved cardiac function by inhibiting oxidative stress and apoptosis in the MI heart. rhFGF21 inhibited both H2O2 and overexpression of ALCAT1-induced oxidative stress and apoptosis by activating the PI3K/AKT pathway in H9C2 cells. In conclusion, our results showed that aerobic exercise alleviated oxidative stress and apoptosis by activating the FGF21/FGFR1/PI3K/AKT pathway or inhibiting the hyperexpression of ALCAT1, which ultimately improved the cardiac function in MI mice.
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