ArticleAmerican journal of physiology. Heart and circulatory physiology2016
Physiological levels of thrombospondin-1 decrease NO-dependent vasodilation in coronary microvessels from aged rats.
Article in American journal of physiology. Heart and circulatory physiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 29 citations in OpenAlex.
- Polycystin-1 suppresses apoptotic signalling in endothelial cells and protects from atherosclerosis.Cardiovascular research · 2026Article
- Endothelial Dysfunction: Redox Imbalance, NLRP3 Inflammasome, and Inflammatory Responses in Cardiovascular Diseases.Antioxidants (Basel, Switzerland) · 2025Review
- Beyond cancer: The potential application of CD47-based therapy in non-cancer diseases.Acta pharmaceutica Sinica. B · 2025Review
- Functional, Structural and Proteomic Effects of Ageing in Resistance Arteries.International journal of molecular sciences · 2024Review
- Tolerating CD47.Clinical and translational medicine · 2024Review
- Molecular mechanisms of endothelial dysfunction in coronary microcirculation dysfunction.Journal of thrombosis and thrombolysis · 2023Review
- Matricellular proteins in atherosclerosis development.Matrix biology : journal of the International Society for Matrix Biology · 2023Review
- Efficient Ex Vivo Screening of Agents Targeting Thrombospondin1-Induced Vascular Dysfunction Using a Digital Multiwire Myograph System.Methods and protocols · 2021Article
- A Potential Role of the CD47/SIRPalpha Axis in COVID-19 Pathogenesis.Current issues in molecular biology · 2021Article
- Thrombospondin 1 in Metabolic Diseases.Frontiers in endocrinology · 2021Review
- CD47 Promotes Age-Associated Deterioration in Angiogenesis, Blood Flow and Glucose Homeostasis.Cells · 2020Article
- Thrombospondin-1 in maladaptive aging responses: a concept whose time has come.American journal of physiology. Cell physiology · 2020Review
- Thrombospondin-1 mediates Drp-1 signaling following ischemia reperfusion in the aging heart.FASEB bioAdvances · 2020Article
- Vascular TSP1-CD47 signaling promotes sickle cell-associated arterial vasculopathy and pulmonary hypertension in mice.American journal of physiology. Lung cellular and molecular physiology · 2019Article
- Lack of thiazide diuretic inhibition of agonist constriction of mouse mesenteric arterioles ex vivo.Naunyn-Schmiedeberg's archives of pharmacology · 2019Article
- Current themes in myocardial and coronary vascular aging.Current opinion in physiology · 2018Article
- Adipose-derived cells improve left ventricular diastolic function and increase microvascular perfusion in advanced age.PloS one · 2018Article
- Thrombospondin-1, Free Radicals, and the Coronary Microcirculation: The Aging Conundrum.Antioxidants & redox signaling · 2017Review
- Regulation of Cellular Redox Signaling by Matricellular Proteins in Vascular Biology, Immunology, and Cancer.Antioxidants & redox signaling · 2017Article
- Matricellular protein thrombospondin-1 in pulmonary hypertension: multiple pathways to disease.Cardiovascular research · 2017Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Aging and cardiovascular disease are associated with the loss of nitric oxide (NO) signaling and a decline in the ability to increase coronary blood flow reserve (CFR). Thrombospondin-1 (Thbs-1), through binding of CD47, has been shown to limit NO-dependent vasodilation in peripheral vascular beds via formation of superoxide (O2 (-)). The present study tests the hypothesis that, similar to the peripheral vasculature, blocking CD47 will improve NO-mediated vasoreactivity in coronary arterioles from aged individuals, resulting in improved CFR. Isolated coronary arterioles from young (4 mo) or old (24 mo) female Fischer 344 rats were challenged with the NO donor, DEA-NONO-ate (1 × 10(-7) to 1 × 10(-4) M), and vessel relaxation and O2 (-) production was measured before and after Thbs-1, αCD47, and/or Tempol and catalase exposure. In vivo CFR was determined in anesthetized rats (1-3% isoflurane-balance O2) via injected microspheres following control IgG or αCD47 treatment (45 min). Isolated coronary arterioles from young and old rats relax similarly to exogenous NO, but addition of 2.2 nM Thbs-1 inhibited NO-mediated vasodilation by 24% in old rats, whereas young vessels were unaffected. Thbs-1 increased O2 (-) production in coronary arterioles from rats of both ages, but this was exaggerated in old rats. The addition of CD47 blocking antibody completely restored NO-dependent vasodilation in isolated arterioles from aged rats and attenuated O2 (-) production. Furthermore, αCD47 treatment increased CFR from 9.6 ± 9.3 (IgG) to 84.0 ± 23% in the left ventricle in intact, aged animals. These findings suggest that the influence of Thbs-1 and CD47 on coronary perfusion increases with aging and may be therapeutically targeted to reverse coronary microvascular dysfunction.
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