{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,30]],"date-time":"2026-07-30T10:47:21Z","timestamp":1785408441701,"version":"3.56.0"},"reference-count":0,"publisher":"Institute of Physiology of the Czech Academy of Sciences","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Physiol Res"],"abstract":"<jats:p>This study aimed to examine the role of hypoxia-inducible factor-1\u03b1 (HIF-1\u03b1) in septic cardiomyopathy (SCM), focusing on its regulatory function in mitochondrial autophagy. Differentially expressed genes (DEGs) associated with SCM were identified through analysis of the GSE79962 dataset. Mitochondrial autophagy-related genes were retrieved from the GeneCards database. Genes common to both datasets were identified using Venn diagram analysis, followed by Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses. A murine model of SCM was established via intraperitoneal injection of lipopolysaccharide (LPS). Mice were subsequently treated with either dimethyloxalylglycine (DMOG) a HIF-1\u03b1 stabilizer, or 3-methyladenine (3-MA), an inhibitor of mitochondrial autophagy. Cardiac function, myocardial injury, inflammatory response, mitochondrial integrity, and expression levels of HIF-1\u03b1 and mitochondrial autophagy markers were assessed using echocardiography, enzyme-linked immunosorbent assay (ELISA), hematoxylin\u2013eosin staining, immunofluorescence, transmission electron microscopy, and western blot analysis. KEGG pathway analysis indicated significant enrichment of the overlapping genes in the HIF-1 signaling pathway. In vivo, DMOG administration stabilized HIF-1\u03b1 expression and upregulated Bcl-2-interacting protein 3 (BNIP3), thereby enhancing mitochondrial autophagy. This enhancement was associated with reduced myocardial enzyme release and inflammatory cytokine production, as well as improvements in mitochondrial ultrastructure, myocardial histopathology, and cardiac function. In contrast, 3-MA inhibited mitochondrial autophagy and attenuated the myocardial protective effects associated with HIF-1\u03b1 stabilization. Activation of the HIF-1\u03b1\/BNIP3 signaling axis promotes mitochondrial autophagy and confers protective on cardiac function in septic cardiomyopathy. These findings present a potential mechanistic pathway and therapeutic target for mitigating myocardial injury associated with septic cardiomyopathy.<\/jats:p>","DOI":"10.33549\/physiolres.935763","type":"journal-article","created":{"date-parts":[[2026,5,18]],"date-time":"2026-05-18T20:10:52Z","timestamp":1779135052000},"page":"301","source":"Crossref","is-referenced-by-count":0,"title":["Hypoxia-Inducible Factor-1\u03b1\/BNIP3-Mediated Mitochondrial Autophagy in Septic Cardiomyopathy: Protective Mechanism for Cardiac Function"],"prefix":"10.33549","author":[{"given":"Q-Q","family":"Liu","sequence":"first","affiliation":[{"id":[{"id":"https:\/\/ror.org\/01mdjbm03","id-type":"ROR","asserted-by":"publisher"}],"name":"Fourth Hospital of Hebei Medical University"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Y-H","family":"Chen","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"C-C","family":"Zhao","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Z-J","family":"Hu","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"19169","published-online":{"date-parts":[[2026,5,12]]},"container-title":["Physiological Research"],"original-title":[],"deposited":{"date-parts":[[2026,5,18]],"date-time":"2026-05-18T20:10:52Z","timestamp":1779135052000},"score":1,"resource":{"primary":{"URL":"https:\/\/www.biomed.cas.cz\/physiolres\/pdf\/2026\/75_301.pdf"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[2026,5,12]]},"references-count":0,"URL":"https:\/\/doi.org\/10.33549\/physiolres.935763","relation":{},"ISSN":["1802-9973"],"issn-type":[{"value":"1802-9973","type":"electronic"}],"subject":[],"published":{"date-parts":[[2026,5,12]]}}}