ArticleExperimental & molecular medicine2022
Cardiac-specific overexpression of Ndufs1 ameliorates cardiac dysfunction after myocardial infarction by alleviating mitochondrial dysfunction and apoptosis.
Article in Experimental & molecular medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.
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Who cites it
54 citing papers in PubMed, 134 citations in OpenAlex.
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- Subthreshold Thermal Stress Aggravates Methamphetamine-Induced Cardiomyocyte Pyroptosis via the Mitochondrial ROS/BAX/mtDNA/NLRP3 Pathway.International journal of molecular sciences · 2026Article
- Identification and Validation of MTFP1 as a Mitochondrial Target Restoring Dynamics and ECM Remodeling in Acute Myocardial Infarction.Current issues in molecular biology · 2026Article
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- Systematic Pharmacology Combined With Experimental Validation Reveals the Apoptosis-Related Mechanism of Simiao Yong'an (SMYA) Decoction Against Myocardial Ischemia-Reperfusion Injury.Cardiovascular therapeutics · 2026Article
- Diagnostic and therapeutic innovations in myocardial infarction: a focus on mitochondrial dysfunction.Frontiers in cardiovascular medicine · 2026Review
- Roles of mitochondrial complexes in non-alcoholic fatty liver disease.Frontiers in molecular biosciences · 2026Review
- Astragaloside IV protects against high altitude hypoxia-induced cardiac injury through the CaSR-NF-kB and EGFR-PI3K-AKT-MDM2 pathways.Apoptosis : an international journal on programmed cell death · 2025Article
- Molecular Insights into Central Core Disease: Proteomic Signatures and Potential Therapeutic Biomarkers in RYR1 I4895T Mice.International journal of molecular sciences · 2025Article
- hsa_circ_0004771-Targeted Adsorption of miR-429 Mediates ATP2A2 Expression to Attenuate Endoplasmic Reticulum Stress and Mitochondrial Dysfunction During Myocardial Infarction.Applied biochemistry and biotechnology · 2025Article
- Rice ragged stunt virus Pns10 induces mitochondrial-mediated apoptosis to promote viral infection in Nilaparvata lugens through disrupting the NlNDUFS1-NlPHB2 interaction.PLoS pathogens · 2025Article
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- Ginsenoside Rg5 alleviates hypoxia-induced myocardial apoptosis by targeting STAT3 to promote Tyr705 phosphorylation.Chinese medicine · 2025Article
- cIAP2-mediated IGF2BP2 ubiquitination and degradation regulate cardiomyocyte apoptosis via stabilizing mCell biology and toxicology · 2025Article
- Isorhamnetin Attenuates Isoproterenol-Induced Myocardial Injury by Reducing ENO1 (Alpha-Enolase) in Cardiomyocytes.Antioxidants (Basel, Switzerland) · 2025Article
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
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Abstract
Myocardial infarction (MI) is the leading cause of premature death among adults. Cardiomyocyte death and dysfunction of the remaining viable cardiomyocytes are the main pathological factors of heart failure after MI. Mitochondrial complexes are emerging as critical mediators for the regulation of cardiomyocyte function. However, the precise roles of mitochondrial complex subunits in heart failure after MI remain unclear. Here, we show that NADH:ubiquinone oxidoreductase core subunit S1 (Ndufs1) expression is decreased in the hearts of heart failure patients and mice with myocardial infarction. Furthermore, we found that cardiac-specific Ndufs1 overexpression alleviates cardiac dysfunction and myocardial fibrosis in the healing phase of MI. Our results demonstrated that Ndufs1 overexpression alleviates MI/hypoxia-induced ROS production and ROS-related apoptosis. Moreover, upregulation of Ndufs1 expression improved the reduced activity of complex I and impaired mitochondrial respiratory function caused by MI/hypoxia. Given that mitochondrial function and cardiomyocyte apoptosis are closely related to heart failure after MI, the results of this study suggest that targeting Ndufs1 may be a potential therapeutic strategy to improve cardiac function in patients with heart failure.
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