ArticleBMC cardiovascular disorders2023
Upgulation of lncRNA GASL1 inhibits atherosclerosis by regulating miR-106a/LKB1 axis.
Article in BMC cardiovascular disorders, 2023. 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.
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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, 5 citations in OpenAlex.
- Uncovering Potential Druggable Targets in Coronary Atherosclerosis: A Proteome-Wide Mendelian Randomization Study With Cross-Platform and Experimental Validation.Cardiovascular therapeutics · 2026Article
- Modulating the Expression of Exercise-induced lncRNAs: Implications for Cardiovascular Disease Progression.Journal of cardiovascular translational research · 2025Review
- LncRNA MAGI2-AS3 promotes the progression of atherosclerosis by sponging miR-525-5p.Journal of cardiothoracic surgery · 2025Article
- LncRNA HOTAIR Inhibits miR-19a-3p to Alleviate Foam Cell Formation and Inflammatory Response in Atherosclerosis.International journal of medical sciences · 2024Article
- Overexpression of TRPV6 Inhibits Coronary Atherosclerosis-Related Inflammatory Response and Cell Apoptosis via the PKA/UCP2 Pathway.Cardiovascular therapeutics · 2024Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAtherosclerosis (AS) is a common frequently-occurring disease in the clinic and a serious threat to human health. This research aimed to explore the value between GASL1 and AS.
methodsThe expression and values of GASL1 in AS patients were revealed by qRT-PCR and ROC curve. The HUVEC cells were induced by ox-LDL to construct in-vitro models. Cell viability was detected by MTT assay, and apoptosis was detected by flow cytometry. The inflammatory situation was reflected by the ELISA assay. Double luciferase reporter gene assay verified the regulatory relationship between GASL1 and miR-106a, miR-106a and LKB1.
resultsThe levels of GASL1 was lower in AS group than those in control group. The value of GASL1 in predicting AS patients was also tested by the ROC curve. After HUVEC cells were induced by ox-LDL, the levels of GASL1 and LKB1 decreased significantly, while the level of miR-106a increased significantly. Upregulation of LKB1 reversed the effect of upregulation of GASL1 on viability, apoptosis, and inflammation of HUVEC cells induced by ox-LDL.
conclusionOverexpression of GASL1 might suppress ox-LDL-induced HUVEC cell viability, apoptosis, and inflammation by regulating miR-106a/LKB1 axis.
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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.