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In vivo and in vitro MIRI models were established. Our results showed that activation of PPAR-\u03b1 decreased the size of the myocardial infarct, maintained cardiac function, and decreased the serum contents of creatine kinase-MB (CK-MB), lactate dehydrogenase (LDH), and Fe\n                    <jats:sup>2+<\/jats:sup>\n                    in ischemia\/reperfusion (I\/R)-treated mice. Additionally, the results of H&amp;E staining, DHE staining, TUNEL staining, and transmission electron microscopy demonstrated that activation of PPAR-\u03b1 inhibited MIRI-induced heart tissue and mitochondrial damage. It was also found that activation of PPAR-\u03b1 attenuated MIRI-induced ferroptosis as shown by a reduction in malondialdehyde, total iron, and reactive oxygen species (ROS). In vitro experiments showed that intracellular contents of malondialdehyde, total iron, LDH, reactive oxygen species (ROS), lipid ROS, oxidized glutathione disulphide (GSSG), and Fe\n                    <jats:sup>2+<\/jats:sup>\n                    were reduced by the activation of PPAR-\u03b1 in H9c2 cells treated with anoxia\/reoxygenation (A\/R), while the cell viability and GSH were increased after PPAR-\u03b1 activation. Additionally, changes in protein levels of the ferroptosis marker further confirmed the beneficial effects of PPAR-\u03b1 activation on MIRI-induced ferroptosis. Moreover, the results of immunofluorescence and dual-luciferase reporter assay revealed that PPAR-\u03b1 achieved its activity via binding to the 14-3-3\u03b7 promoter, promoting its expression level. Moreover, the cardioprotective effects of PPAR-\u03b1 could be canceled by pAd\/14-3-3\u03b7-shRNA or Compound C11 (14-3-3\u03b7 inhibitor). In conclusion, our results indicated that ferroptosis plays a key role in aggravating MIRI, and PPAR-\u03b1\/14-3-3\u03b7 pathway-mediated ferroptosis and mitochondrial injury might be an effective therapeutic target against MIRI.\n                  <\/jats:p>","DOI":"10.1038\/s41598-024-64638-9","type":"journal-article","created":{"date-parts":[[2024,7,2]],"date-time":"2024-07-02T17:01:48Z","timestamp":1719939708000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":19,"title":["Activation of PPAR-\u03b1 attenuates myocardial ischemia\/reperfusion injury by inhibiting ferroptosis and mitochondrial injury via upregulating 14-3-3\u03b7"],"prefix":"10.1038","volume":"14","author":[{"given":"Tie","family":"Hu","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Wen-peng","family":"Yu","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xiu-qi","family":"Wang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Zi-yao","family":"Wang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Zhi-qiang","family":"Xu","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Fa-jia","family":"Hu","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ji-chun","family":"Liu","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Fan","family":"Yu","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Li-jun","family":"Wang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2024,7,2]]},"reference":[{"key":"64638_CR1","doi-asserted-by":"publisher","first-page":"976","DOI":"10.1161\/CIRCULATIONAHA.108.191095","volume":"53","author":"B Surawicz","year":"2009","unstructured":"Surawicz, B. et al. 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