ArticleSleep & breathing = Schlaf & Atmung2019
Mechanisms of vascular endothelial cell injury in response to intermittent and/or continuous hypoxia exposure and protective effects of anti-inflammatory and anti-oxidant agents.
Article in Sleep & breathing = Schlaf & Atmung, 2019. 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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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
10 citing papers in PubMed, 13 citations in OpenAlex.
- Carnosol mitigates Ang II-stimulated vascular injury and oxidative stress by directly binding to FAK and inhibiting its activation.Inflammopharmacology · 2025Article
- Effects of obstructive sleep apnea on myocardial injury and dysfunction: a review focused on the molecular mechanisms of intermittent hypoxia.Sleep & breathing = Schlaf & Atmung · 2024Review
- Cigarette smoke extract stimulates human pulmonary artery smooth muscle cell proliferation: Role of inflammation and oxidative stress.Iranian journal of basic medical sciences · 2022Article
- Comparison of Three Species of Rhubarb in Inhibiting Vascular Endothelial Injury via Regulation of PI3K/AKT/NF-Oxidative medicine and cellular longevity · 2022Article
- Intermittent hypoxia-induced autophagy via AMPK/mTOR signaling pathway attenuates endothelial apoptosis and dysfunction in vitro.Sleep & breathing = Schlaf & Atmung · 2021Article
- Testosterone attenuates hypoxia-induced hypertension by affecting NRF1-mediated transcriptional regulation of ET-1 and ACE.Hypertension research : official journal of the Japanese Society of Hypertension · 2021Article
- Cell-Selective Altered Cargo Properties of Extracellular Vesicles Following In Vitro Exposures to Intermittent Hypoxia.International journal of molecular sciences · 2021Article
- Neuropeptide Y: An Update on the Mechanism Underlying Chronic Intermittent Hypoxia-Induced Endothelial Dysfunction.Frontiers in physiology · 2021Review
- COVID-19: Are we dealing with a multisystem vasculopathy in disguise of a viral infection?Journal of thrombosis and thrombolysis · 2020Review
- Impact of gender differences on prognosis in patients with acute cerebral infarction associated with REM-related obstructive sleep apnea: a retrospective cohort study.Frontiers in neurologyArticle
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundHypoxia induces vascular endothelial injuries; however, the mechanisms involved and effects of interventions remain unclear.
objectiveInvestigate the inflammatory response and oxidative stress in co-cultured neutrophils and vascular endothelial cells, apoptotic changes in endothelial cells, and effects of the antioxidant, Tempol, or the NF-êB inflammatory channel blocker, pyrrolidine dithiocarbamate (PDTC), upon endothelial cells under conditions of intermittent and/or continuous hypoxic exposure.
methodsPolymorphonuclear neutrophils co-cultured with human umbilical vein endothelial cells were subjected to the following conditions: intermittent normoxia (IN), intermittent hypoxia (IH), continuous hypoxia (CH), intermittent with continuous hypoxia (OS), OS+Tempol (OS+T), or OS+PDTC (OS+P) for 2, 5, or 8 h. Inflammatory factors, TNF-α and IL-6, the adhesion molecule, ICAM-1, CAT activity, and MDA concentrations in supernatants from the co-culture as well as pro- (Bak) and anti- (Bcl-xl) apoptotic gene expression levels in the endothelial cells were determined.
resultsInflammatory factors, adhesion molecules, oxidative stress, and apoptosis genes in all groups showed significant, time-dependent increases as compared with the IN group. TNF-α, IL-6, ICAM-1, and MDA levels in the OS group were increased, while CAT was decreased as compared with that observed in the IH, CH, OS+T, and OS+P groups. Bcl-x1 expression and Bcl-x1/BAK ratios were decreased and BAX increased in the OS versus IH, CH, OS+T, or OS+P groups. Both pro- and anti-apoptotic proteins showed time-dependent increases, while the Bcl-x1/BAK ratio decreased over these times. Tempol and PDTC partially prevented these effects.
conclusionInflammation, oxidative stress, and apoptosis are all involved in vascular endothelial injury induced by OS. Anti-inflammatory and anti-oxidative interventions can partially improve effects of OS.
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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.