ArticleDiabetes2015
Direct Endothelial Nitric Oxide Synthase Activation Provides Atheroprotection in Diabetes-Accelerated Atherosclerosis.
Article in Diabetes, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
36 citing papers in PubMed, 70 citations in OpenAlex.
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- Therapeutic role of caveolin family in stem cell fate and development for management of chronic degenerative diseases: A scientometric study to an in-depth review.Journal of advanced research · 2026Review
- Deficiency of neutral cholesterol ester hydrolase 1 (NCEH1) impairs endothelial function in diet-induced diabetic mice.Cardiovascular diabetology · 2024Article
- Endothelial cell CD36 regulates membrane ceramide formation, exosome fatty acid transfer and circulating fatty acid levels.Nature communications · 2023Article
- Role of Echocardiography in Diabetic Cardiomyopathy: From Mechanisms to Clinical Practice.Journal of cardiovascular development and disease · 2023Review
- Ameliorating diabetes-associated atherosclerosis and diabetic nephropathy through modulation of soluble guanylate cyclase.Frontiers in cardiovascular medicine · 2023Article
- Endogenous Protective Factors and Potential Therapeutic Agents for Diabetes-Associated Atherosclerosis.Frontiers in endocrinology · 2022Review
- Red blood cells in type 1 diabetes and multiple sclerosis and technologies to measure their emerging roles.Journal of translational autoimmunity · 2022Review
- Potential Vasculoprotective Effects of Blackcurrant (Molecules (Basel, Switzerland) · 2021Article
- The role of caveolae in endothelial dysfunction.Medical review (2021) · 2021Article
- Early Microvascular Dysfunction: Is the Vasa Vasorum a "Missing Link" in Insulin Resistance and Atherosclerosis.International journal of molecular sciences · 2021Review
- Role of novel biomarkers in diabetic cardiomyopathy.World journal of diabetes · 2021Review
- Pregnancies in Diabetes and Obesity: The Capacity-Load Model of Placental Adaptation.Diabetes · 2021Review
- Effects of citral on serum antioxidant status and liver genes expressions ofIranian journal of veterinary research · 2021Article
- Article
- Role of Caveolin-1 in Diabetes and Its Complications.Oxidative medicine and cellular longevity · 2020Review
- Acacetin Protects Against High Glucose-Induced Endothelial Cells Injury by Preserving Mitochondrial Function via Activating Sirt1/Sirt3/AMPK Signals.Frontiers in pharmacology · 2020Article
- Potential Impact of MicroRNA Gene Polymorphisms in the Pathogenesis of Diabetes and Atherosclerotic Cardiovascular Disease.Journal of personalized medicine · 2019Review
- Sildenafil Prevents Marfan-Associated Emphysema and Early Pulmonary Artery Dilation in Mice.The American journal of pathology · 2019Article
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Authors and funding
10 authors at 4 institutions in 2 countries.
Funding
Abstract
Patients with diabetes have an increased risk of developing atherosclerosis. Endothelial dysfunction, characterized by the lowered bioavailability of endothelial NO synthase (eNOS)-derived NO, is a critical inducer of atherosclerosis. However, the protective aspect of eNOS in diabetes-associated atherosclerosis remains controversial, a likely consequence of its capacity to release both protective NO or deleterious oxygen radicals in normal and disease settings, respectively. Harnessing the atheroprotective activity of eNOS in diabetic settings remains elusive, in part due to the lack of endogenous eNOS-specific NO release activators. We have recently shown in vitro that eNOS-derived NO release can be increased by blocking its binding to Caveolin-1, the main coat protein of caveolae, using a highly specific peptide, CavNOxin. However, whether targeting eNOS using this peptide can attenuate diabetes-associated atherosclerosis is unknown. In this study, we show that CavNOxin can attenuate atherosclerotic burden by ∼84% in vivo. In contrast, mice lacking eNOS show resistance to CavNOxin treatment, indicating eNOS specificity. Mechanistically, CavNOxin lowered oxidative stress markers, inhibited the expression of proatherogenic mediators, and blocked leukocyte-endothelial interactions. These data are the first to show that endogenous eNOS activation can provide atheroprotection in diabetes and suggest that CavNOxin is a viable strategy for the development of antiatherosclerotic compounds.
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Registered trials
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.