ReviewJournal of applied physiology (Bethesda, Md. : 1985)2011
Ca2+ regulatory mechanisms of exercise protection against coronary artery disease in metabolic syndrome and diabetes.
Review in Journal of applied physiology (Bethesda, Md. : 1985), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
What it found
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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.
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Who cites it
31 citing papers in PubMed, 51 citations in OpenAlex.
- Article
- A new model of heart failure with preserved ejection fraction induced by metabolic syndrome in Ossabaw miniature swine.Basic research in cardiology · 2025Article
- Regular Exercise Rescues Heart Function Defects and Shortens the Lifespan ofInternational journal of environmental research and public health · 2022Article
- Exercise Training and Interventions for Coronary Artery Disease.Journal of cardiovascular development and disease · 2022Review
- Intracellular CaJournal of cardiovascular translational research · 2022Article
- The Endothelium as a Therapeutic Target in Diabetes: A Narrative Review and Perspective.Frontiers in physiology · 2021Review
- Long-term incidence of cardiovascular outcomes in the middle-aged and elderly with different patterns of physical activity: Tehran lipid and glucose study.BMC public health · 2020Article
- Endurance exercise training does not limit coronary atherosclerosis in familial hypercholesterolemic swine.Physiological reports · 2019Article
- Effect of metabolic syndrome and aging on CaExperimental gerontology · 2018Article
- Physical Activity in the Prevention and Treatment of Coronary Artery Disease.Journal of the American Heart Association · 2018Review
- 17β-estradiol reduces CaPharmacology research & perspectives · 2017Article
- Exercise, oxidants, and antioxidants change the shape of the bell-shaped hormesis curve.Redox biology · 2017Article
- Intracellular calcium increases in vascular smooth muscle cells with progression of chronic kidney disease in a rat model.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2017Article
- Biphasic alterations in coronary smooth muscle Ca(2+) regulation in a repeat cross-sectional study of coronary artery disease severity in metabolic syndrome.Atherosclerosis · 2016Article
- Leptin augments coronary vasoconstriction and smooth muscle proliferation via a Rho-kinase-dependent pathway.Basic research in cardiology · 2016Article
- Göttingen minipig model of diet-induced atherosclerosis: influence of mild streptozotocin-induced diabetes on lesion severity and markers of inflammation evaluated in obese, obese and diabetic, and lean control animals.Journal of translational medicine · 2015Article
- Metabolic Syndrome Abolishes Glucagon-Like Peptide 1 Receptor Agonist Stimulation of SERCA in Coronary Smooth Muscle.Diabetes · 2015Article
- Shock wave lithotripsy does not impair renal function in a Swine model of metabolic syndrome.Journal of endourology · 2015Article
- Exercise training reduces insulin resistance in postmyocardial infarction rats.Physiological reports · 2015Article
- Noninvasive assessment of pulse-wave velocity and flow-mediated vasodilation in anesthetized Göttingen minipigs.Comparative medicine · 2014Article
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
Chronic exercise attenuates coronary artery disease (CAD) in humans largely independent of reductions in risk factors; thus major protective mechanisms of exercise are directly within the coronary vasculature. Further, tight control of diabetes, e.g., blood glucose, can be detrimental. Accordingly, knowledge of mechanisms by which exercise attenuates diabetic CAD could catalyze development of molecular therapies. Exercise attenuates CAD (atherosclerosis) and restenosis in miniature swine models, which enable precise control of exercise parameters (intensity, duration, and frequency) and characterization of the metabolic syndrome (MetS) and diabetic milieu. Intracellular Ca(2+) is a pivotal second messenger for coronary smooth muscle (CSM) excitation-contraction and excitation-transcription coupling that modulates CSM proliferation, migration, and calcification. CSM of diabetic dyslipidemic Yucatan swine have impaired Ca(2+) extrusion via the plasmalemma Ca(2+) ATPase (PMCA), downregulation of L-type voltage-gated Ca(2+) channels (VGCC), increased Ca(2+) sequestration by the sarcoplasmic reticulum (SR) Ca(2+) ATPase (SERCA), increased nuclear Ca(2+) localization, and greater activation of K channels by Ca(2+) release from the SR. Endurance exercise training prevents Ca(2+) transport changes with virtually no effect on the diabetic milieu (glucose, lipids). In MetS Ossabaw swine transient receptor potential canonical (TRPC) channels are upregulated and exercise training reverses expression and TRPC-mediated Ca(2+) influx with almost no change in the MetS milieu. Overall, exercise effects on Ca(2+) signaling modulate CSM phenotype. Future studies should 1) selectively target key Ca(2+) transporters to determine definitively their causal role in atherosclerosis and 2) combine mechanistic studies with clinical outcomes, e.g., reduction of myocardial infarction.
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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.