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.

• Authors: 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
• Journal: iScience (iScience) Vol. 25 Issue 6 Pg. 104447 (Jun 17 2022) ISSN: 2589-0042 [Electronic] United States
• PMID: 35707727 (Publication Type: Journal Article)
• Copyright: © 2022 The Author(s).