ArticleBasic research in cardiology2023
Reduction in mitochondrial ROS improves oxidative phosphorylation and provides resilience to coronary endothelium in non-reperfused myocardial infarction.
Article in Basic research in cardiology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
34 citing papers in PubMed, 54 citations in OpenAlex.
- Molecular Mechanisms Governing Vascular Function in Heart Failure.Arteriosclerosis, thrombosis, and vascular biology · 2026Review
- Live Visualization of Endoplasmic Reticulum Redox Potential in Zebrafish Embryos Reveals Region-Specific Heterogeneity.Biomedicines · 2026Article
- Engineered Tan-CDs@AS-IV Nanosystem Orchestrates Mitochondrial Biogenesis and Intercellular Transfer to Restore Endothelial Function via PGC-1α and Cx43 Signaling Pathways.Nanomaterials (Basel, Switzerland) · 2026Article
- Betulin Protects Against Cardiac Hypertrophy by Improving AMPK/Nrf2-Dependent Mitochondrial Function.Phytotherapy research : PTR · 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
- CircPDXDC1 Induces Mitochondrial Dysfunction and Autophagy Dysfunction in Acute Myocardial Infarction by Promoting ELAVL1 Ubiquitination.Applied biochemistry and biotechnology · 2026Article
- EV-Encapsulated Mitochondrial miRNAs: Enhancing Cardiomyocyte Bioenergetics.International journal of molecular sciences · 2026Review
- NLGN3 contributes to angiogenesis in myocardial infarction via activation of the Gαi1/3-Akt pathway.Basic research in cardiology · 2026Article
- Suppression of USP2 in mouse skeletal muscle: a model of oxidative stress in muscle tissue.Experimental animals · 2026Article
- Uncovering mitochondrial dynamics-related genes as potential diagnostic biomarkers for acute myocardial infarction.Frontiers in cardiovascular medicine · 2026Article
- Oxycodone: A Pain-Relieving Agent With Cardioprotective Properties Against Myocardial Ischemia-Reperfusion Injury.Cardiovascular therapeutics · 2026Review
- Bioinformatics Identification and Experimental Validation of Ferroptosis- and Immune Infiltration-Associated Biomarkers in Ischemic Stroke.Current issues in molecular biology · 2025Article
- Advancing diabetic foot ulcer therapy: structure-activity relationship approaches for combating reactive oxygen species.Molecular biology reports · 2025Review
- Nuclear Lactate Dehydrogenase A Resists Cardiomyocyte Cell Cycle Arrest Induced by Oxidative Stress.Journal of cardiovascular development and disease · 2025Article
- Manganese Superoxide Dismutase: Structure, Function, and Implications in Human Disease.Antioxidants (Basel, Switzerland) · 2025Review
- Sivelestat-Loaded Neutrophil-Membrane-Coated Antioxidative Nanoparticles for Targeted Endothelial Protection in Sepsis.Pharmaceutics · 2025Article
- Preventive and Therapeutic Effects of Sericin-Derived Oligopeptides (SDOs) from Yellow Silk Cocoons on Blood Pressure Lowering in L-NAME-Induced Hypertensive Rats.Foods (Basel, Switzerland) · 2025Article
- Early microvascular coronary endothelial dysfunction precedes pembrolizumab-induced cardiotoxicity. Preventive role of high dose of atorvastatin.Basic research in cardiology · 2025Article
- Lab-grown, 3D extracellular matrix particles improve cardiac function and morphology in myocardial ischemia.American journal of physiology. Heart and circulatory physiology · 2025Article
- Nanomaterials: Promising Tools for the Diagnosis and Treatment of Myocardial Infarction.International journal of nanomedicine · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
Recent studies demonstrated that mitochondrial antioxidant MnSOD that reduces mitochondrial (mito) reactive oxygen species (ROS) helps maintain an optimal balance between sub-cellular ROS levels in coronary vascular endothelial cells (ECs). However, it is not known whether EC-specific mito-ROS modulation provides resilience to coronary ECs after a non-reperfused acute myocardial infarction (MI). This study examined whether a reduction in endothelium-specific mito-ROS improves the survival and proliferation of coronary ECs in vivo. We generated a novel conditional binary transgenic animal model that overexpresses (OE) mitochondrial antioxidant MnSOD in an EC-specific manner (MnSOD-OE). EC-specific MnSOD-OE was validated in heart sections and mouse heart ECs (MHECs). Mitosox and mito-roGFP assays demonstrated that MnSOD-OE resulted in a 50% reduction in mito-ROS in MHEC. Control and MnSOD-OE mice were subject to non-reperfusion MI surgery, echocardiography, and heart harvest. In post-MI hearts, MnSOD-OE promoted EC proliferation (by 2.4 ± 0.9 fold) and coronary angiogenesis (by 3.4 ± 0.9 fold), reduced myocardial infarct size (by 27%), and improved left ventricle ejection fraction (by 16%) and fractional shortening (by 20%). Interestingly, proteomic and Western blot analyses demonstrated upregulation in mitochondrial complex I and oxidative phosphorylation (OXPHOS) proteins in MnSOD-OE MHECs. These MHECs also showed increased mitochondrial oxygen consumption rate (OCR) and membrane potential. These findings suggest that mito-ROS reduction in EC improves coronary angiogenesis and cardiac function in non-reperfused MI, which are associated with increased activation of OXPHOS in EC-mitochondria. Activation of an energy-efficient mechanism in EC may be a novel mechanism to confer resilience to coronary EC during MI.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.