Identification of metabolic pathways underlying FGF1 and CHIR99021-mediated cardioprotection

Bing Xu; Fan Li; Wenjing Zhang; Yajuan Su; Ling Tang; Pengsheng Li; Jyotsna Joshi; Aaron Yang; Dong Li; Zhao Wang; Shu Wang; Jingwei Xie; Haiwei Gu; Wuqiang Zhu

doi:10.1016/j.isci.2022.104447

Identification of metabolic pathways underlying FGF1 and CHIR99021-mediated cardioprotection

Bing Xu, Fan Li, Wenjing Zhang, Yajuan Su, Ling Tang, Pengsheng Li, Jyotsna Joshi, Aaron Yang, Dong Li, Zhao Wang, Shu Wang, Jingwei Xie, Haiwei Gu, Wuqiang Zhu

Cardiovascular Diseases

Research output: Contribution to journal › Article › peer-review

Abstract

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.

Original language	English (US)
Article number	104447
Journal	iScience
Volume	25
Issue number	6
DOIs	https://doi.org/10.1016/j.isci.2022.104447
State	Published - Jun 17 2022

Keywords

Health sciences
Nanotechnology
Omics

ASJC Scopus subject areas

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10.1016/j.isci.2022.104447

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title = "Identification of metabolic pathways underlying FGF1 and CHIR99021-mediated cardioprotection",

abstract = "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.",

keywords = "Health sciences, Nanotechnology, Omics",

author = "Bing Xu and Fan Li and Wenjing Zhang and Yajuan Su and Ling Tang and Pengsheng Li and Jyotsna Joshi and Aaron Yang and Dong Li and Zhao Wang and Shu Wang and Jingwei Xie and Haiwei Gu and Wuqiang Zhu",

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doi = "10.1016/j.isci.2022.104447",

language = "English (US)",

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AU - Xu, Bing

AU - Li, Fan

AU - Zhang, Wenjing

AU - Su, Yajuan

AU - Tang, Ling

AU - Li, Pengsheng

AU - Joshi, Jyotsna

AU - Yang, Aaron

AU - Li, Dong

AU - Wang, Zhao

AU - Wang, Shu

AU - Xie, Jingwei

AU - Gu, Haiwei

AU - Zhu, Wuqiang

PY - 2022/6/17

Y1 - 2022/6/17

N2 - 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.

AB - 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.

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KW - Omics

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Identification of metabolic pathways underlying FGF1 and CHIR99021-mediated cardioprotection

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