ArticleMedical science monitor : international medical journal of experimental and clinical research2014
Reactive oxygen species contribute to simulated ischemia/reperfusion-induced autophagic cell death in human umbilical vein endothelial cells.
Article in Medical science monitor : international medical journal of experimental and clinical research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 17 citations in OpenAlex.
- Programmed Cell Death of Endothelial Cells in Ischemic Heart Disease: Mechanism and Potential Cell and Gene Therapeutic Prospects.Bioengineering (Basel, Switzerland) · 2026Review
- Comprehensive molecular and cellular characterization of endoplasmic reticulum stress-related key genes in renal ischemia/reperfusion injury.Frontiers in immunology · 2024Article
- New Dawn for Atherosclerosis: Vascular Endothelial Cell Senescence and Death.International journal of molecular sciences · 2023Review
- rTFPI Protects Cardiomyocytes from Hypoxia/Reoxygenation Injury through Inhibiting Autophagy and the Class III PI3K/Beclin-1 Pathway.Cell biochemistry and biophysics · 2023Article
- Madder (Mediators of inflammation · 2023Article
- Tetramethylpyrazine Protects Endothelial Injury and Antithrombosis via Antioxidant and Antiapoptosis in HUVECs and Zebrafish.Oxidative medicine and cellular longevity · 2022Article
- MicroRNA-155 affects oxidative damage through regulating autophagy in endothelial cells.Oncology letters · 2019Article
- Mechanisms of autophagy activation in endothelial cell and their targeting during normothermic machine liver perfusion.World journal of gastroenterology · 2017Review
- Simulated ischemia/reperfusion-induced p65-Beclin 1-dependent autophagic cell death in human umbilical vein endothelial cells.Scientific reports · 2016Article
- Assessment of the effect of laser irradiations at different wavelengths (660, 810, 980, and 1064 nm) on autophagy in a rat model of mucositis.Lasers in medical science · 2015Article
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAutophagy is important for cells to degrade protein aggregates and organelles. Our preliminary study suggests that ischemia/reperfusion in rabbit hearts promoted autophagic myocardial injury, resulting in no-reflow phenomenon. In this study, we sought to further understand the mechanism and outcome of the upregulation of autophagy in ischemia/reperfusion. MATERIAL AND
methodsWe employed a simulated ischemia/reperfusion (sI/R) model in human umbilical vein endothelial cells (HUVECs) in vitro, in the presence or absence of antioxidants.
resultsOur study confirms that sI/R induces autophagy in HUVECs as measured by increased expression of Beclin 1 and microtubule-associated protein 1 light chain 3 (LC3), electron microscopic analysis, and special biofluorescent staining with monodansylcadaverine. This sI/R-induced autophagy was also accompanied by increased levels of p65 protein expression and cell death. In addition, we detected the accumulation of reactive oxygen species (ROS) after sI/R. Moreover, with the application of ROS scavengers that block the release of ROS, we were able to demonstrate that inhibition of autophagy increases cell survival.
conclusionsThe study suggests that ROS accumulation is involved in the sI/R-induced autophagic cell death in HUVECs.
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