ArticlePloS one2014
Loss of Sirt3 limits bone marrow cell-mediated angiogenesis and cardiac repair in post-myocardial infarction.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed.
- Microvascular Rarefaction in the Sinoatrial Node: A Potential Mechanism for Pacemaker Dysfunction in Early HFpEF.JACC. Clinical electrophysiology · 2025Article
- The life cycle of a capillary: Mechanisms of angiogenesis and rarefaction in microvascular physiology and pathologies.Vascular pharmacology · 2024Review
- Article
- Redox Homeostasis in Cardiovascular Disease: The Role of Mitochondrial Sirtuins.Frontiers in endocrinology · 2022Review
- Article
- Gene Expression Profiling of Multiple Histone Deacetylases (Biomolecules · 2020Article
- Sirtuin (Sirt) 3 Overexpression Prevents Retinopathy in Streptozotocin-Induced Diabetic Rats.Medical science monitor : international medical journal of experimental and clinical research · 2020Article
- The Role of Sirtuin 3 in Radiation-Induced Long-Term Persistent Liver Injury.Antioxidants (Basel, Switzerland) · 2020Article
- Sirtuin 3 deficiency does not impede digit regeneration in mice.Scientific reports · 2019Article
- Emerging role of SIRT3 in endothelial metabolism, angiogenesis, and cardiovascular disease.Journal of cellular physiology · 2019Review
- Microvascular Rarefaction and Heart Failure With Preserved Ejection Fraction.Frontiers in cardiovascular medicine · 2019Review
- PCB11 Metabolite, 3,3'-Dichlorobiphenyl-4-ol, Exposure Alters the Expression of Genes Governing Fatty Acid Metabolism in the Absence of Functional Sirtuin 3: Examining the Contribution of MnSOD.Antioxidants (Basel, Switzerland) · 2018Article
- Sirtuins and NADCirculation research · 2018Review
- Sirt3 deficiency impairs neurovascular recovery in ischemic stroke.CNS neuroscience & therapeutics · 2018Article
- The effect of oxygen in Sirt3-mediated myocardial protection: a proof-of-concept study in cultured cardiomyoblasts.Journal of thrombosis and thrombolysis · 2018Article
- Genetic and Functional Sequence Variants of the SIRT3 Gene Promoter in Myocardial Infarction.PloS one · 2016Article
- The role of sirtuins in cardiac disease.American journal of physiology. Heart and circulatory physiology · 2015Review
- Apelin Gene Therapy Increases AutophagyDiabetes research (Fairfax, Va.) · 2015Article
- Critical Roles of Reactive Oxygen Species in Age-Related Impairment in Ischemia-Induced Neovascularization by Regulating Stem and Progenitor Cell Function.Oxidative medicine and cellular longevity · 2015Review
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3 authors.
Funding
Abstract
Sirtuin-3 (Sirt3) has a critical role in the regulation of human aging and reactive oxygen species (ROS) formation. A recent study has identified Sirt3 as an essential regulator of stem cell aging. This study investigated whether Sirt3 is necessary for bone marrow cell (BMC)-mediated cardiac repair in post-myocardial infarction (MI). In vitro, BMC-derived endothelial progenitor cells (EPCs) from wild type (WT) and Sirt3KO mice were cultured. EPC angiogenesis, ROS formation and apoptosis were assessed. In vivo, WT and Sirt3 KO mice were subjected to MI and BMCs from WT and Sirt3 KO mice were injected into ischemic area immediately. The expression of VEGF and VEGFR2 was reduced in Sirt3KO-EPCs. Angiogenic capacities and colony formation were significantly impaired in Sirt3KO-EPCs compared to WT-EPCs. Loss of Sirt3 further enhanced ROS formation and apoptosis in EPCs. Overexpression of Sirt3 or treatment with NADPH oxidase inhibitor apocynin (Apo, 200 and 400 microM) rescued these abnormalities. In post-MI mice, BMC treatment increased number of Sca1+/c-kit+ cells; enhanced VEGF expression and angiogenesis whereas Sirt3KO-BMC treatment had little effects. BMC treatment also attenuated NADPH oxidase subunits p47phox and gp91phox expression, and significantly reduced ROS formation, apoptosis, fibrosis and hypertrophy in post-MI mice. Sirt3KO-BMC treatment did not display these beneficial effects. In contrast, Sirt3KO mice treated with BMCs from WT mice attenuated myocardial apoptosis, fibrosis and improved cardiac function. Our data demonstrate that Sirt3 is essential for BMC therapy; and loss of Sirt3 limits BMC-mediated angiogenesis and cardiac repair in post-MI.
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