ArticleCanadian journal of physiology and pharmacology2014
Impairment of autophagy in endothelial cells prevents shear-stress-induced increases in nitric oxide bioavailability.
Article in Canadian journal of physiology and pharmacology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 79 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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Who cites it
79 citing papers in PubMed, 124 citations in OpenAlex.
- Bryostatin-1 improves function in arteries with suppressed endothelial cell autophagy.GeroScience · 2026Article
- Endothelial Cell Autophagy Suppresses Metastasis In Mouse Mammary and Pancreatic Neuroendocrine Tumor Models.bioRxiv : the preprint server for biology · 2026Article
- miR-320a Regulates Placenta Endothelial Function After Fetal Cardiopulmonary Bypass via the ATG7-SIRT1/FOXO1 Pathway.Current medical science · 2025Article
- Targeting Gut Microbiota to Combat Vascular Aging and Cardiovascular Disease: Mechanisms and Therapeutic Potential.Nutrients · 2025Review
- The multifaceted role of autophagy and mitophagy in cardiovascular health and disease.Autophagy reports · 2025Review
- Everolimus alleviates CD4GeroScience · 2024Article
- Autophagy in Muscle Regeneration: Mechanisms, Targets, and Therapeutic Perspective.International journal of molecular sciences · 2024Review
- Role of ROS and autophagy in the pathological process of atherosclerosis.Journal of physiology and biochemistry · 2024Review
- Autophagy as a Guardian of Vascular Niche Homeostasis.International journal of molecular sciences · 2024Review
- Nrf2 Connects Cellular Autophagy and Vascular Senescence in Atherosclerosis: A Mini-Review.Journal of lipid and atherosclerosis · 2024Review
- Elucidating the crosstalk between endothelial-to-mesenchymal transition (EndoMT) and endothelial autophagy in the pathogenesis of atherosclerosis.Vascular pharmacology · 2024Review
- Review
- Autophagy Behavior in Endothelial Cell Regeneration.Current aging science · 2024Review
- Mitochondria in health, disease, and aging.Physiological reviews · 2023Review
- Autophagy-urea cycle pathway is essential for the statin-mediated nitric oxide bioavailability in endothelial cells.Journal of food and drug analysis · 2023Article
- Autophagy in Heart Failure: Insights into Mechanisms and Therapeutic Implications.Journal of cardiovascular development and disease · 2023Review
- Proteostasis and resilience in the mechanically-stressed vascular endothelium.Current opinion in physiology · 2023Review
- Autophagy protein 5 controls flow-dependent endothelial functions.Cellular and molecular life sciences : CMLS · 2023Article
- Molecular regulation and therapeutic implications of cell death in pulmonary hypertension.Cell death discovery · 2023Review
- Caveolin-1 and Atherosclerosis: Regulation of LDLs Fate in Endothelial Cells.International journal of molecular sciences · 2023Review
19 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 1 institution in 1 country.
Funding
Abstract
Autophagy is a lysosomal catabolic process by which cells degrade or recycle their contents to maintain cellular homeostasis, adapt to stress, and respond to disease. Impairment of autophagy in endothelial cells studied under static conditions results in oxidant stress and impaired nitric oxide (NO) bioavailability. We tested the hypothesis that vascular autophagy is also important for induction of NO production caused by exposure of endothelial cells to shear stress (i.e., 3 h × ≈20 dyn/cm(2)). Atg3 is a requisite autophagy pathway mediator. Control cells treated with non-targeting control siRNA showed increased autophagy, reactive oxygen species (ROS) production, endothelial NO synthase (eNOS) phosphorylation, and NO production upon exposure to shear stress (p < 0.05 for all). In contrast, cells with >85% knockdown of Atg3 protein expression (via Atg3 siRNA) exhibited a profound impairment of eNOS phosphorylation, and were incapable of increasing NO in response to shear stress. Moreover, ROS accumulation and inflammatory cytokine production (MCP-1 and IL-8) were exaggerated (all p < 0.05) in response to shear stress. These findings reveal that autophagy not only plays a critical role in maintaining NO bioavailability, but may also be a key regulator of oxidant-antioxidant balance and inflammatory-anti-inflammatory balance that ultimately regulate endothelial cell responses to shear stress.
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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.