ArticleOxidative medicine and cellular longevity2017
Inhibition of Caveolae Contributes to Propofol Preconditioning-Suppressed Microvesicles Release and Cell Injury by Hypoxia-Reoxygenation.
Article in Oxidative medicine and cellular longevity, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 19 citations in OpenAlex.
- Influence of Anesthetic Regimes on Extracellular Vesicles following Remote Ischemic Preconditioning in Coronary Artery Disease.International journal of molecular sciences · 2024Trial
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- VSNL1 attenuates hypoxia‑induced myocardial apoptosis by regulating the CNP/NPRB pathway.Molecular medicine reports · 2026Article
- Ginsenoside Rb1 Alleviated the AKI to CKD Transition by Targeting VEGFR2.Journal of cellular and molecular medicine · 2025Article
- Propofol inhibits myocardial injury induced by microvesicles derived from hypoxia-reoxygenated endothelial cells via lncCCT4-2/CCT4 signaling.Biological research · 2023Article
- Propionate alleviates myocardial ischemia-reperfusion injury aggravated by Angiotensin II dependent on caveolin-1/ACE2 axis through GPR41.International journal of biological sciences · 2022Article
- Inhibition of lncRNA NEAT1 protects endothelial cells against hypoxia/reoxygenation‑induced NLRP3 inflammasome activation by targeting the miR‑204/BRCC3 axis.Molecular medicine reports · 2022Article
- Propofol protects hippocampal neurons in sleep-deprived rats by inhibiting mitophagy and autophagy.Annals of translational medicine · 2021Article
- 4-Methoxybenzylalcohol protects brain microvascular endothelial cells against oxygen-glucose deprivation/reperfusion-induced injury via activation of the PI3K/AKT signaling pathway.Experimental and therapeutic medicine · 2021Article
- Extracellular vesicles: Potential impact on cardiovascular diseases.Advances in clinical chemistry · 2021Review
- Hypoxia-Inducible Factor-1: A Potential Target to Treat Acute Lung Injury.Oxidative medicine and cellular longevity · 2020Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Endothelial microvesicles (EMVs), released after endothelial cell (EC) apoptosis or activation, may carry many adverse signals and propagate injury by intercellular transmission. Caveolae are 50-100 nm cell surface plasma membrane invaginations involved in many pathophysiological processes. Recent evidence has indicated EMVs and caveolae may have functional effects in cells undergoing H/R injury. Propofol, a widely used anaesthetic, confers antioxidative stress capability in the same process. But the connection between EMVs, H/R, and caveolae remains largely unclear. Here, we found that H/R significantly increased the release of EMVs, the expression of CAV-1 (the structural protein responsible for maintaining the shape of caveolae), oxidative stress, and the mitochondrial damage, and all these changes were inhibited by propofol preconditioning. Interestingly, the caveolae inhibitor M
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