ArticleBMC cardiovascular disorders2015
Role of SIRT3 in Angiotensin II-induced human umbilical vein endothelial cells dysfunction.
Article in BMC cardiovascular disorders, 2015. 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, 35 citations in OpenAlex.
- Advances in the Role of SIRT3 in Vascular Remodeling in Hypertension.Biomolecules · 2026Review
- Modulation of sirtuin expression by a high-sugar diet and regular swimming trained precedes the loss of kidney function.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2025Article
- miRNA-142-3p aggravates hydrogen peroxide-induced human umbilical vein endothelial cell premature senescence by targeting SIRT1.Bioscience reports · 2024Article
- Gastrodin alleviates premature senescence of vascular endothelial cells by enhancing the Nrf2/HO-1 signalling pathway.Journal of cellular and molecular medicine · 2024Article
- Theories and Molecular Basis of Vascular Aging: A Review of the Literature from VascAgeNet Group on Pathophysiological Mechanisms of Vascular Aging.International journal of molecular sciences · 2022Review
- SIRT3 attenuates coronary atherosclerosis in diabetic patients by regulating endothelial cell function.Journal of clinical laboratory analysis · 2022Article
- Intratubular, Intracellular, and Mitochondrial Angiotensin II/ATFrontiers in physiology · 2021Review
- Microglia mediated neuroinflammation - signaling regulation and therapeutic considerations with special reference to some natural compounds.Histology and histopathology · 2020Review
- Angiotensin II Decreases Endothelial Nitric Oxide Synthase PhosphorylationFrontiers in physiology · 2020Article
- Sirtuin 3, Endothelial Metabolic Reprogramming, and Heart Failure With Preserved Ejection Fraction.Journal of cardiovascular pharmacology · 2019Review
- Emerging role of SIRT3 in endothelial metabolism, angiogenesis, and cardiovascular disease.Journal of cellular physiology · 2019Review
- Where Metabolism Meets Senescence: Focus on Endothelial Cells.Frontiers in physiology · 2019Review
- Microvascular Rarefaction and Heart Failure With Preserved Ejection Fraction.Frontiers in cardiovascular medicine · 2019Review
- Endothelial specific SIRT3 deletion impairs glycolysis and angiogenesis and causes diastolic dysfunction.Journal of molecular and cellular cardiology · 2017Article
- Trimethylamine-N-Oxide Induces Vascular Inflammation by Activating the NLRP3 Inflammasome Through the SIRT3-SOD2-mtROS Signaling Pathway.Journal of the American Heart Association · 2017Article
- Sirtuin 3 Deficiency Accelerates Hypertensive Cardiac Remodeling by Impairing Angiogenesis.Journal of the American Heart Association · 2017Article
- Sirtuins, Cell Senescence, and Vascular Aging.The Canadian journal of cardiology · 2016Review
- SIRT3 Deficiency Induces Endothelial Insulin Resistance and Blunts Endothelial-Dependent Vasorelaxation in Mice and Human with Obesity.Scientific reports · 2016Article
- TNFα-Damaged-HUVECs Microparticles Modify Endothelial Progenitor Cell Functional Activity.Frontiers in physiology · 2015Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundSIRT3, a member of the sirtuin family of NAD(+)-dependent deacetylases, resides primarily in the mitochondria and has been shown to deacetylate several metabolic and respiratory enzymes that regulate important mitochondrial functions. Previous researches show an important role of SIRT3 in regulating the production of reactive oxygen species (ROS), and highlight the ability of SIRT3 to protect cells from oxidative damage. A key substance of renin-angiotensin-aldosterone system (RAAS), Angiotensin II (AngII) can induce cells dysfunction by increasing the production of ROS. In this paper, we focus on the role of SIRT3 in AngII-induced human umbilical vein endothelial cells (HUVECs) dysfunction.
methodsTo study the influence of AngII on SIRT3 expression, HUVECs were treated with AngII of 10(-7), 10(-6), 10(-5) mol/L for 24 h. SIRT3 expression was detected by wester-blotting analysis and RT-PCR. In addition, to research the role of SIRT3 in AngII-induced HUVECs,we used SIRT3 siRNA to knock down SIRT3 expression in HUVECs. Cells pretreated with negative control siRNA or SIRT3 siRNA were exposed to AngII for 24 h, and endothelial nitric oxide synthase (eNOS) expression, eNOS activity, total level of nitric oxide (NO) and ROS generation of each group were detected.
resultsHere we show that AngII treatment could increase generation of ROS, and decrease eNOS activity and total level of NO, while upregulated eNOS expression as a compensatory mechanism. The stimulation of AngII upregulated the expression of SIRT3 in HUVECs. SIRT3 siRNA worsen the AngII-induced effects above, besides, downregulated eNOS protein expression.
conclusionThese data suggest that SIRT3 plays a role of protection in AngII-induced HUVECs dysfunction via regulation of ROS generation.
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