ArticleProceedings of the National Academy of Sciences of the United States of America2017
Electron leak from NDUFA13 within mitochondrial complex I attenuates ischemia-reperfusion injury via dimerized STAT3.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 60 citations in OpenAlex.
- STAT3 suppresses palmitic acid-induced apoptosis and fatty acid oxidation dysfunction in bovine mammary epithelial cells by transcriptionally activating CPT1A.Science China. Life sciences · 2026Article
- Moderate downregulation of NDUFA13 promotes cardiomyocytes proliferation and heart regeneration through the glycolysis/c‑Myc/International journal of molecular medicine · 2026Article
- Article
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- Mitochondrial electron transport chain gene-based prognostic model identifies SDHB as a key regulator of low-grade glioma progression and therapeutic target.Cancer cell international · 2025Article
- Map-based cloning of ZmSS5, construction and validation of its regulatory pathway for maize kernel weight.TAG. Theoretical and applied genetics. Theoretische und angewandte Genetik · 2025Article
- Mitochondrial Quality Control in Health and Disease.MedComm · 2025Review
- Donor Age Impairs Vasculogenic Potential of hiPSC-Derived Endothelial Progenitors.bioRxiv : the preprint server for biology · 2025Article
- Changes in the Proteomic Profile After Audiogenic Kindling in the Inferior Colliculus of the GASH/Sal Model of Epilepsy.International journal of molecular sciences · 2025Article
- Machine learning analysis of gene expression profiles of pyroptosis-related differentially expressed genes in ischemic stroke revealed potential targets for drug repurposing.Scientific reports · 2025Article
- SGK3 deficiency in macrophages suppresses angiotensin II-induced cardiac remodeling via regulating Ndufa13-mediated mitochondrial oxidative stress.Cellular and molecular life sciences : CMLS · 2024Article
- Integration of virtual screening and proteomics reveals potential targets and pathways for ginsenoside RgJournal of ginseng research · 2024Article
- Mitochondrial GRIM19 Loss Induces Liver Fibrosis through NLRP3/IL33 Activation via Reactive Oxygen Species/NF-кB Signaling.Journal of clinical and translational hepatology · 2024Article
- Mitochondrial transport of catalytic RNAs and targeting of the organellar transcriptome in human cells.Journal of molecular cell biology · 2024Article
- Exogeneous metal ions as therapeutic agents in cardiovascular disease and their delivery strategies.Regenerative biomaterials · 2024Review
- Small and Large Extracellular Vesicles Derived from Pleural Mesothelioma Cell Lines Offer Biomarker Potential.Cancers · 2023Article
- Identification of mClinical epigenetics · 2023Article
- Short-Term Blockade of Pro-Inflammatory Alarmin S100A9 Favorably Modulates Left Ventricle Proteome and Related Signaling Pathways Involved in Post-Myocardial Infarction Recovery.International journal of molecular sciences · 2022Article
- Identification of Lactate-Related Gene Signature for Prediction of Progression and Immunotherapeutic Response in Skin Cutaneous Melanoma.Frontiers in oncology · 2022Article
- Regulation of STAT3 and its role in cardioprotection by conditioning: focus on non-genomic roles targeting mitochondrial function.Basic research in cardiology · 2021Review
Corrections and comments
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Authors and funding
15 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The causative relationship between specific mitochondrial molecular structure and reactive oxygen species (ROS) generation has attracted much attention. NDUFA13 is a newly identified accessory subunit of mitochondria complex I with a unique molecular structure and a location that is very close to the subunits of complex I of low electrochemical potentials. It has been reported that down-regulated NDUFA13 rendered tumor cells more resistant to apoptosis. Thus, this molecule might provide an ideal opportunity for us to investigate the profile of ROS generation and its role in cell protection against apoptosis. In the present study, we generated cardiac-specific tamoxifen-inducible NDUFA13 knockout mice and demonstrated that cardiac-specific heterozygous knockout (cHet) mice exhibited normal cardiac morphology and function in the basal state but were more resistant to apoptosis when exposed to ischemia-reperfusion (I/R) injury. cHet mice showed a preserved capacity of oxygen consumption rate by complex I and II, which can match the oxygen consumption driven by electron donors of
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