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Published on: June 3, 2018
Fibroblast Growth Factor 18 Regulates Mitochondrial Function to Alleviate Myocardial Ischemia-Reperfusion Injury in
Haijiao Yang1, Guanglei He2, Xiaojing Cui3
1Department of Coronary Care Unit, Yantaishan Hospital, Yantai, China.
DNA and Cell Biology
|June 16, 2026
Summary
Fibroblast growth factor 18 (FGF18) protects against myocardial ischemia-reperfusion injury (MIRI) by improving mitochondrial function and reducing oxidative stress via the SIRT1/PGC-1α pathway.
Area of Science:
- Cardiovascular Research
- Mitochondrial Biology
- Molecular Medicine
Background:
- Myocardial ischemia-reperfusion injury (MIRI) is a significant clinical challenge.
- Mitochondrial dysfunction and oxidative stress are key contributors to MIRI pathogenesis.
- The Sirtuin 1/peroxisome proliferator-activated receptor gamma coactivator 1 (SIRT1/PGC-1α) pathway plays a crucial role in mitochondrial homeostasis.
Purpose of the Study:
- To investigate the role of fibroblast growth factor 18 (FGF18) in rat MIRI.
- To elucidate the involvement of the SIRT1/PGC-1α pathway in FGF18's protective effects.
- To determine FGF18's impact on mitochondrial function and oxidative stress during MIRI.
Main Methods:
- Established rat MIRI models with FGF18 knockdown and overexpression.
- Utilized an in vitro hypoxia-reoxygenation (H/R) model with H9c2 cardiomyocytes.
- Administered SIRT1 inhibitor EX-527 to FGF18-overexpressing cells.
- Assessed infarct size, cardiomyocyte injury, mitochondrial parameters, oxidative stress markers, and protein expression (FGF18, SIRT1, PGC-1α, Mfn1).
- Performed immunoprecipitation and protein acetylation assays to evaluate PGC-1α acetylation.
Main Results:
- FGF18 overexpression improved mitochondrial function, reduced oxidative stress, and enhanced cell survival in MIRI and H/R models.
- FGF18 knockdown exacerbated MIRI and H/R-induced damage.
- FGF18 upregulated SIRT1/PGC-1α/Mfn1 expression and inhibited PGC-1α acetylation.
- SIRT1 inhibition abolished the protective effects of FGF18.
- FGF18 regulates PGC-1α acetylation through SIRT1-mediated deacetylation.
Conclusions:
- FGF18 exerts protective effects against rat myocardial MIRI.
- FGF18 attenuates MIRI by alleviating oxidative stress and maintaining mitochondrial homeostasis.
- The mechanism involves FGF18-mediated regulation of the SIRT1/PGC-1α pathway, specifically SIRT1-dependent deacetylation of PGC-1α.
