ArticleAging2013
Oxidative stress improves coronary endothelial function through activation of the pro-survival kinase AMPK.
Article in Aging, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 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.
The trial behind it
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
42 citing papers in PubMed, 74 citations in OpenAlex.
- Sigma 1 Receptor Activation Coordinates Metabolic Stress Responses to Protect Retinal Vasculature in Ischemic Retinopathy.Investigative ophthalmology & visual science · 2026Article
- Role of Matricellular Proteins in Endothelial Cell Inflammation and Atherosclerosis.Antioxidants (Basel, Switzerland) · 2025Review
- Pequi (Antioxidants (Basel, Switzerland) · 2025Article
- Protective Roles and Therapeutic Effects of Gallic Acid in the Treatment of Cardiovascular Diseases: Current Trends and Future Directions.Current medicinal chemistry · 2024Review
- Reduction in mitochondrial ROS improves oxidative phosphorylation and provides resilience to coronary endothelium in non-reperfused myocardial infarction.Basic research in cardiology · 2023Article
- Coronary Microvascular Dysfunction in Diabetes Mellitus: Pathogenetic Mechanisms and Potential Therapeutic Options.Biomedicines · 2022Review
- Factors and Pathways Modulating Endothelial Cell Senescence in Vascular Aging.International journal of molecular sciences · 2022Review
- Review
- Mechanisms and clinical implications of endothelium-dependent vasomotor dysfunction in coronary microvasculature.American journal of physiology. Heart and circulatory physiology · 2022Review
- Lack of Endothelial α1AMPK Reverses the Vascular Protective Effects of Exercise by Causing eNOS Uncoupling.Antioxidants (Basel, Switzerland) · 2021Article
- Hepatocyte-specific suppression of ANGPTL4 improves obesity-associated diabetes and mitigates atherosclerosis in mice.The Journal of clinical investigation · 2021Article
- Delivery of a mitochondria-targeted antioxidant from biocompatible, polymeric nanofibrous scaffolds.FEBS open bio · 2021Article
- Coronary endothelial dysfunction prevented by small-conductance calcium-activated potassium channel activator in mice and patients with diabetes.The Journal of thoracic and cardiovascular surgery · 2020Article
- The Relationship Between Reactive Oxygen Species and Endothelial Cell Metabolism.Frontiers in chemistry · 2020Review
- Endothelial Nanomechanics in the Context of Endothelial (Dys)function and Inflammation.Antioxidants & redox signaling · 2019Review
- Downregulation of G2/mitotic-specific cyclinB1 triggers autophagy via AMPK-ULK1-dependent signal pathway in nasopharyngeal carcinoma cells.Cell death & disease · 2019Article
- The Synergistic Effect of Nanocrystals Combined With Ultrasound in the Generation of Reactive Oxygen Species for Biomedical Applications.Frontiers in bioengineering and biotechnology · 2019Article
- MTHFD1L-Mediated Redox Homeostasis Promotes Tumor Progression in Tongue Squamous Cell Carcinoma.Frontiers in oncology · 2019Article
- MicroRNA‑155 promotes ox‑LDL‑induced autophagy in human umbilical vein endothelial cells by targeting the PI3K/Akt/mTOR pathway.Molecular medicine reports · 2018Article
- Subcellular Reactive Oxygen Species (ROS) in Cardiovascular Pathophysiology.Antioxidants (Basel, Switzerland) · 2018Review
Corrections and comments
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Authors and funding
14 authors at 4 institutions in 3 countries.
Funding
Abstract
Age-associated decline in cardiovascular function is believed to occur from the deleterious effects of reactive oxygen species (ROS). However, failure of recent clinical trials using antioxidants in patients with cardiovascular disease, and the recent findings showing paradoxical role for NADPH oxidase-derived ROS in endothelial function challenge this long-held notion against ROS. Here, we examine the effects of endothelium-specific conditional increase in ROS on coronary endothelial function. We have generated a novel binary (Tet-ON/OFF) conditional transgenic mouse (Tet-Nox2:VE-Cad-tTA) that induces endothelial cell (EC)-specific overexpression of Nox2/gp91 (NADPH oxidase) and 1.8?0.42-fold increase in EC-ROS upon tetracycline withdrawal (Tet-OFF). We examined ROS effects on EC signaling and function. First, we demonstrate that endothelium-dependent coronary vasodilation was significantly improved in Tet-OFF Nox2 compared to Tet-ON (control) littermates. Using EC isolated from mouse heart, we show that endogenous ROS increased eNOS activation and nitric oxide (NO) synthesis through activation of the survival kinase AMPK. Coronary vasodilation in Tet-OFF Nox2 animals was CaMKK?-AMPK-dependent. Finally, we demonstrate that AMPK activation induced autophagy and thus, protected ECs from oxidant-induced cell death. Together, these findings suggest that increased ROS levels, often associated with cardiovascular conditions in advanced age, play a protective role in endothelial homeostasis by inducing AMPK-eNOS axis.
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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.