ArticleAmerican journal of physiology. Heart and circulatory physiology2014
The SIRT1 activator SRT1720 reverses vascular endothelial dysfunction, excessive superoxide production, and inflammation with aging in mice.
Article in American journal of physiology. Heart and circulatory physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 108 papers.
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Who cites it
108 citing papers in PubMed, 176 citations in OpenAlex.
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- Elucidate senescence-related gene signature and immune infiltration landscape in abdominal aortic aneurysm.PloS one · 2026Article
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- Arterial stiffness and vascular aging: mechanisms, prevention, and therapy.Signal transduction and targeted therapy · 2025Review
- Systemic aging fuels heart failure: Molecular mechanisms and therapeutic avenues.ESC heart failure · 2025Review
- Endothelial Dysfunction: Redox Imbalance, NLRP3 Inflammasome, and Inflammatory Responses in Cardiovascular Diseases.Antioxidants (Basel, Switzerland) · 2025Review
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- Oxidative stress and its related epigenetic modifications in vascular calcification: mechanisms and advances.Frontiers in cardiovascular medicine · 2025Review
- Declining nitric oxide bioavailability in cardiovascular aging: mechanistic insights and emerging interventions.The journal of cardiovascular aging · 2025Article
- Is postoperative cognitive dysfunction a disease of microglial inflammatory memory? A state-transition model from metabolic stress to epigenetic lock-in.Frontiers in molecular neuroscience · 2025Review
- Role of AMPK and Sirtuins in Aging Heart: Basic and Translational Aspects.Aging and disease · 2024Review
- Review
- Mitochondrial dysfunction in the pathogenesis of endothelial dysfunction.Molecular and cellular biochemistry · 2024Review
- Novel Techniques, Biomarkers and Molecular Targets to Address Cardiometabolic Diseases.Journal of clinical medicine · 2024Review
- Aging in Ocular Blood Vessels: Molecular Insights and the Role of Oxidative Stress.Biomedicines · 2024Review
48 more citing papers are in PubMed but not listed here.
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Authors and funding
6 authors at 1 institution in 1 country.
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Abstract
Reductions in arterial SIRT1 expression and activity with aging are linked to vascular endothelial dysfunction. We tested the hypothesis that the specific SIRT1 activator SRT1720 improves endothelial function [endothelium-dependent dilation (EDD)] in old mice. Young (4-9 mo) and old (29-32 mo) male B6D2F1 mice treated with SRT1720 (100 mg/kg body wt) or vehicle for 4 wk were studied with a group of young controls. Compared with the young controls, aortic SIRT1 expression and activity were reduced (P < 0.05) and EDD was impaired (83 ± 2 vs. 96 ± 1%; P < 0.01) in old vehicle-treated animals. SRT1720 normalized SIRT1 expression/activity in old mice and restored EDD (95 ± 1%) by enhancing cyclooxygenase (COX)-2-mediated dilation and protein expression in the absence of changes in nitric oxide bioavailability. Aortic superoxide production and expression of NADPH oxidase 4 (NOX4) were increased in old vehicle mice (P < 0.05), and ex vivo administration of the superoxide scavenger TEMPOL restored EDD in that group. SRT1720 normalized aortic superoxide production in old mice, without altering NOX4 and abolished the improvement in EDD with TEMPOL, while selectively increasing aortic antioxidant enzymes. Aortic nuclear factor-κB (NF-κB) activity and tumor necrosis factor-α (TNF-α) were increased in old vehicle mice (P < 0.05), whereas SRT1720 normalized NF-κB activation and reduced TNF-α in old animals. SIRT1 activation with SRT1720 ameliorates vascular endothelial dysfunction with aging in mice by enhancing COX-2 signaling and reducing oxidative stress and inflammation. Specific activation of SIRT1 is a promising therapeutic strategy for age-related endothelial dysfunction in humans.
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