ArticleCardiovascular drugs and therapy2021
Reduction in MicroRNA-4488 Expression Induces NFκB Translocation in Venous Endothelial Cells Under Arterial Flow.
Article in Cardiovascular drugs and therapy, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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
6 citing papers in PubMed, 9 citations in OpenAlex.
- A microRNA generated via lysosomal processing of ribosomal RNA suppresses proinflammatory responses.Life science alliance · 2026Article
- Postmortem analyses of myocardial microRNA expression in sepsis.Scientific reports · 2024Observational
- Serum miR-4488 as a potential biomarker of lean nonalcoholic fatty liver disease.Annals of translational medicine · 2023Article
- Autologous Platelet-Rich Growth Factor Reduces M1 Macrophages and Modulates Inflammatory Microenvironments to Promote Sciatic Nerve Regeneration.Biomedicines · 2022Article
- Sodium phenylbutyrate inhibits Schwann cell inflammation via HDAC and NFκB to promote axonal regeneration and remyelination.Journal of neuroinflammation · 2021Article
- Extracellular vesicles from immortalized cardiosphere-derived cells attenuate arrhythmogenic cardiomyopathy in desmoglein-2 mutant mice.European heart journal · 2021Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeLittle is known about the molecular interactions among inflammatory responses that damage venous endothelial cells (vECs) during venous-to-arterial flow transition in vein graft diseases. Because arterial flow triggers excessive autophagy and inflammation in vECs, this study aimed to investigate the mediator of inflammation and methods to prevent vEC damage.
methodsArterial laminar shear stress (ALSS; 12 dynes/cm
resultsALSS triggered reactive oxygen species production, excessive autophagy, COX-2 protein expression, and NFκB translocation during vEC inflammation. Reduction in miR-4488 expression was detected in inflamed vECs treated with LPS, lipopolysaccharide (LPS) TNFα, and ALSS. Transfection of miR-4488 mimic (50 nM) prior to ALSS application inhibited the accumulation of inflammatory proteins as well as the translocation of NFκB. Combined treatment of vECs with COX-2-specific inhibitor (SC-236) and L-Arg alleviated the ALSS-induced inflammatory responses. Protective effects of the combined treatment on vECs against ALSS-induced damage were abolished by the application of miR-4488 inhibitor.
conclusionWe showed that ALSS triggered the COX-2/NFκB pathway to induce vEC inflammation with a reduction in miR-4488. Combination of SC-236 and L-Arg prevented ALSS-induced vEC damage, thus, shows high potential for preventing vein graft diseases.
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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.