ArticleAmerican journal of physiology. Regulatory, integrative and comparative physiology2020
Effect of endoplasmic reticulum stress on endothelial ischemia-reperfusion injury in humans.
Article in American journal of physiology. Regulatory, integrative and comparative physiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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
5 citing papers in PubMed, 7 citations in OpenAlex.
- Acute heat exposure protects against endothelial ischemia-reperfusion injury in aged humans.American journal of physiology. Regulatory, integrative and comparative physiology · 2022Article
- Shear stress induced by acute heat exposure is not obligatory to protect against endothelial ischemia-reperfusion injury in humans.Journal of applied physiology (Bethesda, Md. : 1985) · 2022Article
- Improving the ischemia-reperfusion injury in vascularized composite allotransplantation: Clinical experience and experimental implications.Frontiers in immunology · 2022Review
- Influence of ischemia-reperfusion injury on endothelial function in men and women with similar serum estradiol concentrations.American journal of physiology. Regulatory, integrative and comparative physiology · 2021Article
- Novel Insight into the Role of Endoplasmic Reticulum Stress in the Pathogenesis of Myocardial Ischemia-Reperfusion Injury.Oxidative medicine and cellular longevity · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Endoplasmic reticulum stress contributes to ischemia-reperfusion (I/R) injury in rodent and cell models. However, the contribution of endoplasmic reticulum stress in the pathogenesis of endothelial I/R injury in humans is unknown. We tested the hypothesis that compared with placebo, inhibition of endoplasmic reticulum stress via ingestion of tauroursodeoxycholic acid would prevent the attenuation of endothelium-dependent vasodilation following I/R injury. Twelve young adults (6 women) were studied following ingestion of a placebo or 1,500 mg tauroursodeoxycholic acid (TUDCA). Endothelium-dependent vasodilation was assessed via brachial artery flow-mediated dilation (duplex ultrasonography) before and after I/R injury, which was induced by 20 min of arm ischemia followed by 20 min of reperfusion. Endothelium-independent vasodilation (glyceryl trinitrate-mediated vasodilation) was also assessed after I/R injury. Compared with placebo, TUDCA ingestion increased circulating plasma concentrations by 145 ± 90 ng/ml and increased concentrations of the taurine unconjugated form, ursodeoxycholic acid, by 560 ± 156 ng/ml (both
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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.