GDF15 attenuates myocardial infarction-induced injury by preserving mitochondrial function and suppressing oxidative stress.
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ABSTRACT: Myocardial infarction, a serious cardiovascular disease, is still a major cause of morbidity and mortality worldwide. Growth differentiation factor-15, a stress-responsive cytokine, has been involved in cardiac pathophysiology, but its exact role in myocardial infarction remains controversial. This study aimed to clarify the mechanisms underlying the cardioprotective effects of GDF-15 in myocardial infarction. By using a combination of in vivo and in vitro methods, including immunofluorescence staining, echocardiography, RNA sequencing, and high-resolution respirometry, we showed that GDF-15 expression is significantly upregulated in infarcted myocardium and its deficiency aggravates cardiac injury. Mechanistically, GDF-15 deficiency impairs mitochondrial function and energy metabolism und
SUBMITTER: Yuan X
PROVIDER: S-EPMC12482560 | biostudies-literature | 2025 Sep
REPOSITORIES: biostudies-literature
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