ArticleAmerican journal of translational research2020
Simvastatin ameliorates oxygen glucose deprivation/reoxygenation-induced pulmonary endothelial barrier dysfunction by restoring cell-cell junctions and actin cytoskeleton dynamics via the PI3K/Akt signaling pathway.
Article in American journal of translational research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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
3 citing papers in PubMed.
- Patient-specific iPSC-derived ECs identify QKI-7 as a key regulator of endothelial dysfunction and potential therapeutic target in diabetes.Stem cells translational medicine · 2026Article
- Natural products as HMG-CoA reductase inhibitors (statins) for the management of non-communicable diseases.Inflammopharmacology · 2026Review
- Review
Corrections and comments
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Endothelial barrier dysfunction is a critical pathophysiological process of pulmonary ischemia/reperfusion (I/R) injury in patients scheduled for cardiopulmonary bypass. Impaired actin cytoskeleton dynamics and cell-cell junctions are the main causes of endothelial dysfunction. Statins have protective effects on I/R-induced lung injury; however, the mechanism is unclear. We explored the therapeutic potential of simvastatin (SV) in endothelial cells subjected to oxygen-glucose deprivation/reoxygenation (OGD/R). SV pretreatment promoted the barrier function of human pulmonary microvascular endothelial cells (HPMECs) subjected to OGD/R. LY294002 was used to evaluate the role of the PI3K/Akt pathway in regulating the barrier function of HPMECs subjected to OGD/R. LY294002 suppressed the barrier function of HPMECs. SV restored the endothelial barrier function by rescuing endothelial cell migration and permeability, which are involved in the regulation of cytoskeleton dynamics and intercellular junction expression via the PI3K/Akt signaling pathway.
Indexed as
Identifiers
33042440PMC7540106What OpenQuestion holds
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.