Identification of metabolic pathways underlying FGF1 and CHIR99021-mediated cardioprotection.
Identification of metabolic pathways underlying FGF1 and CHIR99021-mediated cardioprotection.
复制标题
确定成纤维细胞生长因子1（FGF1）和CHIR99021介导的心脏保护作用的代谢途径。
DOI：
10.1016/j.isci.2022.104447
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发表时间：
2022-06-17
期刊：
影响因子：
5.8
通讯作者：
Zhu, Wuqiang
中科院分区：
文献类型：
--
作者：
Xu, Bing;Li, Fan;Zhang, Wenjing;Su, Yajuan;Tang, Ling;Li, Pengsheng;Joshi, Jyotsna;Yang, Aaron;Li, Dong;Wang, Zhao;Wang, Shu;Xie, Jingwei;Gu, Haiwei;Zhu, Wuqiang
急性心肌梗死是全球主要的死亡原因。我们先前已经确定了两种心脏保护分子——成纤维细胞生长因子1（FGF1）和CHIR99021，它们在小鼠和猪的急性心肌梗死模型中具有心脏保护作用。在此，我们旨在确定心肌代谢的改善是否有助于这种心脏保护作用。在手术诱导心肌梗死后，立即将负载FGF1和CHIR99021的纳米纤维心肌内注射到成年小鼠的缺血心肌中。在3天和7天后对动物实施安乐死。我们的数据表明，FGF1/CHIR99021纳米纤维增强了心脏利用糖酵解作为能量来源的能力，并减少了缺血心肌中支链氨基酸的积累。FGF1/CHIR99021对代谢的影响在心肌梗死后的前三天更为明显。综上所述，这些发现表明FGF1/CHIR99021通过改善心肌代谢来保护心脏免受缺血损伤，这可能被用于人类急性心肌梗死的治疗。
FGF1/CHIR在心肌梗死动物中具有心脏保护作用
FGF1/CHIR增强缺血心脏通过糖酵解产生能量的能力
FGF1/CHIR减少缺血心脏中支链氨基酸的含量
这项研究揭示了一种纠正缺血心脏代谢紊乱的新方法
健康科学；纳米技术；组学
Acute myocardial infarction is a leading cause of death worldwide. We have previously identified two cardioprotective molecules — FGF1 and CHIR99021— that confer cardioprotection in mouse and pig models of acute myocardial infarction. Here, we aimed to determine if improved myocardial metabolism contributes to this cardioprotection. Nanofibers loaded with FGF1 and CHIR99021 were intramyocardially injected to ischemic myocardium of adult mice immediately following surgically induced myocardial infarction. Animals were euthanized 3 and 7 days later. Our data suggested that FGF1/CHIR99021 nanofibers enhanced the heart’s capacity to utilize glycolysis as an energy source and reduced the accumulation of branched-chain amino acids in ischemic myocardium. The impact of FGF1/CHIR99021 on metabolism was more obvious in the first three days post myocardial infarction. Taken together, these findings suggest that FGF1/CHIR99021 protects the heart against ischemic injury via improving myocardial metabolism which may be exploited for treatment of acute myocardial infarction in humans. FGF1/CHIR confer cardioprotection in myocardial infarction animals FGF1/CHIR enhance the capability of ischemic hearts to produce energy via glycolysis FGF1/CHIR reduce the abundance of branched chain amino acids in ischemic hearts This study reveals a novel approach to correct metabolic disorders in ischemic hearts Health sciences; Nanotechnology; Omics
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DOI：
10.1042/bcj20200656
发表时间：
2020-11-27
期刊：
The Biochemical journal
影响因子：
--
作者：
Fernandes PM;Kinkead J;McNae I;Michels PAM;Walkinshaw MD
通讯作者：
Walkinshaw MD
影响因子：
8
作者：
Fan, Chengming;Oduk, Yasin;Zhang, Jianyi
通讯作者：
Zhang, Jianyi
影响因子：
9.5
作者：
Chan, Brandon Y. H.;Roczkowsky, Andrej;Schulz, Richard
通讯作者：
Schulz, Richard
影响因子：
2.9
作者：
Cole JT;Sweatt AJ;Hutson SM
通讯作者：
Hutson SM
影响因子：
8.8
作者：
Dai C;Li Q;May HI;Li C;Zhang G;Sharma G;Sherry AD;Malloy CR;Khemtong C;Zhang Y;Deng Y;Gillette TG;Xu J;Scadden DT;Wang ZV
通讯作者：
Wang ZV