ArticleBasic research in cardiology2026
Mitochondrial bioenergetics deficit linked to endothelial dysfunction and ER stress induced by obesity in coronary arteries.
Article in Basic research in cardiology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Obesity and metabolic syndrome are major drivers of metabolic heart disease, characterized by profound cardiac energy deficits, structural remodeling, and progression to heart failure. While myocardial mitochondrial dysfunction in obesity is well established, its impact on coronary arteries remains underexplored. This study investigates how high-fat diet (HFD)-induced obesity affects coronary bioenergetics, mitochondrial REDOX balance, and endothelial function. Male Wistar rats were fed a HFD (60% kcal fat) for 15-16 weeks after weaning as a model of diet-induced obesity, and tunicamycin-treated rats as a model of chemically-induced ER stress in vivo were used. Myograph experiments to assess coronary endothelial function, reactive oxygen species (ROS) measurements, and mitochondrial respiration experiments in a Seahorse analyzer were comprehensively conducted. After 15-16 weeks of HFD rats developed metabolic syndrome features, including weight gain, hyperglycemia, hypertriglyceridemia, and elevated lactate. Coronary arteries exhibited endothelial dysfunction, evidenced by impaired acetylcholine- and isoprenaline-induced relaxations, mediated by NADPH oxidase 1 (NOX1)-derived ROS, as selective NOX1 inhibition (NoxA1ds-tat) restored vasodilation. Mitochondrial ROS (mtROS) levels increased in arteries but not myocardium, along with preserved hydrogen peroxide (H
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