ArticleYonsei medical journal2018
Effects of Antioxidant Tempol on Systematic Inflammation and Endothelial Apoptosis in Emphysematous Rats Exposed to Intermittent Hypoxia.
Article in Yonsei medical journal, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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
7 citing papers in PubMed, 9 citations in OpenAlex.
- Obstructive sleep apnea and lung cancer: molecular underpinnings and clinical translational prospects.Frontiers in cell and developmental biology · 2026Review
- Polymorphonuclear neutrophils promote endothelial apoptosis by enhancing adhesion upon stimulation by intermittent hypoxia.Sleep & breathing = Schlaf & Atmung · 2022Article
- Decreased expression of PPARγ is associated with aortic endothelial cell apoptosis in intermittently hypoxic rats.Sleep & breathing = Schlaf & Atmung · 2021Article
- Beneficial Effect of Tempol, a Membrane-Permeable Radical Scavenger, on Inflammation and Osteoarthritis in In Vitro Models.Biomolecules · 2021Article
- Neuropeptide Y: An Update on the Mechanism Underlying Chronic Intermittent Hypoxia-Induced Endothelial Dysfunction.Frontiers in physiology · 2021Review
- Could Adjunctive Pharmacology Mitigate Cardiovascular Consequences of Obstructive Sleep Apnea?American journal of respiratory and critical care medicine · 2019Article
- 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.Sleep & breathing = Schlaf & Atmung · 2019Article
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
purposeObstructive sleep apnea and chronic obstructive pulmonary disease are independent risk factors of cardiovascular disease (CVD), and their coexistence is known as overlap syndrome (OS). Endothelial dysfunction is the initial stage of CVD; however, underlying mechanisms linking OS and CVD are not well understood. The aim of this study was to explore whether OS can lead to more severe inflammation and endothelial apoptosis by promoting endothelial dysfunction, and to assess the intervention effects of antioxidant tempol. MATERIALS AND
methodsMale Wistar rats (n=66) were exposed to normal oxygen [normal control (NC) group], intermittent hypoxia (IH group), cigarette smoke (CH group), as well as cigarette smoke and IH (OS group). Tempol intervention was assessed in OS group treated with tempol (OST group) or NaCl (OSN group). After an 8-week challenge, lung tissues, serum, and fresh blood were harvested for analysis of endothelial markers and apoptosis.
resultsThe levels of intracellular adhesion molecule-1, vascular cellular adhesion molecule-1, and apoptosis in circulating epithelial cells were the highest in OS group and the lowest in NC group. These levels were all greater in IH group than in CH group, and were lower in OST group than in OS and OSN groups (all
conclusionSynergistic effects of IH with cigarette smoke-induced emphysema produce a greater inflammatory status and endothelial apoptosis. OS-related inflammation and endothelial cell apoptosis may play important roles in promoting cardiovascular dysfunction, and antioxidant tempol could achieve a partial protective effect.
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