ArticleBasic research in cardiology2016
Impaired coronary metabolic dilation in the metabolic syndrome is linked to mitochondrial dysfunction and mitochondrial DNA damage.
Article in Basic research in cardiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 38 citations in OpenAlex.
- From kidney injury to cardiac dysfunction: the central role of oxidative stress in diabetes and CKD.Basic research in cardiology · 2026Article
- Diagnostic and therapeutic innovations in myocardial infarction: a focus on mitochondrial dysfunction.Frontiers in cardiovascular medicine · 2026Review
- A robust method for assessing mitochondrial function in healthy and diseased frozen cardiac tissue.Communications biology · 2025Article
- Emerging roles of the acid sphingomyelinase/ceramide pathway in metabolic and cardiovascular diseases: Mechanistic insights and therapeutic implications.World journal of cardiology · 2025Review
- Impaired endothelial function contributes to cardiac dysfunction: role of mitochondrial dynamics.American journal of physiology. Heart and circulatory physiology · 2025Review
- Platelet bioenergetics correlate with skeletal muscle respiration in a murine model of type II diabetes.Frontiers in molecular biosciences · 2025Article
- Recent advances associated with cardiometabolic remodeling in diabetes-induced heart failure.American journal of physiology. Heart and circulatory physiology · 2024Review
- Novel Strategies in the Early Detection and Treatment of Endothelial Cell-Specific Mitochondrial Dysfunction in Coronary Artery Disease.Antioxidants (Basel, Switzerland) · 2023Review
- Impairment of Mitochondrial Respiration in Metabolic Diseases: An Overview.International journal of molecular sciences · 2022Review
- Noncanonical Role of Telomerase in Regulation of Microvascular Redox Environment With Implications for Coronary Artery Disease.Function (Oxford, England) · 2022Article
- Experimental animal models of coronary microvascular dysfunction.Cardiovascular research · 2020Review
- Perturbations in myocardial perfusion and oxygen balance in swine with multiple risk factors: a novel model of ischemia and no obstructive coronary artery disease.Basic research in cardiology · 2020Article
- Cardioprotection during ischemia by coronary collateral growth.American journal of physiology. Heart and circulatory physiology · 2019Review
- Chemotherapeutic-Induced Cardiovascular Dysfunction: Physiological Effects, Early Detection-The Role of Telomerase to Counteract Mitochondrial Defects and Oxidative Stress.International journal of molecular sciences · 2018Review
- Hyperoxia Causes Mitochondrial Fragmentation in Pulmonary Endothelial Cells by Increasing Expression of Pro-Fission Proteins.Arteriosclerosis, thrombosis, and vascular biology · 2018Article
- Regulation of myocardial oxygen delivery in response to graded reductions in hematocrit: role of KBasic research in cardiology · 2017Article
- Influence of increased heart rate and aortic pressure on resting indices of functional coronary stenosis severity.Basic research in cardiology · 2017Article
- EET intervention on Wnt1, NOV, and HO-1 signaling prevents obesity-induced cardiomyopathy in obese mice.American journal of physiology. Heart and circulatory physiology · 2017Article
- Transition in the mechanism of flow-mediated dilation with aging and development of coronary artery disease.Basic research in cardiology · 2017Article
- Severe familial hypercholesterolemia impairs the regulation of coronary blood flow and oxygen supply during exercise.Basic research in cardiology · 2016Article
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Authors and funding
16 authors at 6 institutions in 4 countries.
Funding
Abstract
Mitochondrial dysfunction in obesity and diabetes can be caused by excessive production of free radicals, which can damage mitochondrial DNA. Because mitochondrial DNA plays a key role in the production of ATP necessary for cardiac work, we hypothesized that mitochondrial dysfunction, induced by mitochondrial DNA damage, uncouples coronary blood flow from cardiac work. Myocardial blood flow (contrast echocardiography) was measured in Zucker lean (ZLN) and obese fatty (ZOF) rats during increased cardiac metabolism (product of heart rate and arterial pressure, i.v. norepinephrine). In ZLN increased metabolism augmented coronary blood flow, but in ZOF metabolic hyperemia was attenuated. Mitochondrial respiration was impaired and ROS production was greater in ZOF than ZLN. These were associated with mitochondrial DNA (mtDNA) damage in ZOF. To determine if coronary metabolic dilation, the hyperemic response induced by heightened cardiac metabolism, is linked to mitochondrial function we introduced recombinant proteins (intravenously or intraperitoneally) in ZLN and ZOF to fragment or repair mtDNA, respectively. Repair of mtDNA damage restored mitochondrial function and metabolic dilation, and reduced ROS production in ZOF; whereas induction of mtDNA damage in ZLN reduced mitochondrial function, increased ROS production, and attenuated metabolic dilation. Adequate metabolic dilation was also associated with the extracellular release of ADP, ATP, and H2O2 by cardiac myocytes; whereas myocytes from rats with impaired dilation released only H2O2. In conclusion, our results suggest that mitochondrial function plays a seminal role in connecting myocardial blood flow to metabolism, and integrity of mtDNA is central to this process.
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