ArticleExperimental and therapeutic medicine2021
miR-454-3p prevents ox-LDL-induced apoptosis in HAECs by targeting TRPC3.
Article in Experimental and therapeutic medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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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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Who cites it
6 citing papers in PubMed, 7 citations in OpenAlex.
- Pre-transplant microRNA serum profiles and association with acute graft-versus-host disease in allogeneic hematopoietic stem cell transplantation.Frontiers in immunology · 2026Article
- Article
- Platelet microRNA Expression Can Predict Bleeding in HeartMate3 Patients Treated With or Without Aspirin.Journal of cardiovascular translational research · 2025Observational
- Tan IIA mitigates vascular smooth muscle cell proliferation and migration induced by ox-LDL through the miR-137/TRPC3 axis.The Kaohsiung journal of medical sciences · 2023Article
- The Potential Role of MiRs-139-5p and -454-3p in Endoglin-Knockdown-Induced Angiogenic Dysfunction in HUVECs.International journal of molecular sciences · 2023Article
- Comprehensive Analysis of a Competing Endogenous RNA Co-Expression Network in Chronic Obstructive Pulmonary Disease.International journal of chronic obstructive pulmonary disease · 2023Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Endothelial-cell (EC) apoptosis serves a vital role in the pathogenesis of atherosclerosis. Accumulating evidence has implicated microRNA (miRNA/miR) dysregulation in EC apoptosis. Although the role of miR-454-3p in carcinogenesis has been well documented, its role and underlying mechanism in EC apoptosis remain unclear. In the present study, the results revealed that miR-454-3p expression was substantially downregulated in human aortic endothelial cells (HAECs) following oxidized low-density lipoprotein (ox-LDL) treatment. miR-454-3p suppression significantly attenuated the viability of HAECs, while miR-454-3p overexpression repressed ox-LDL-induced HAEC apoptosis. Bioinformatics analysis and luciferase reporter assays revealed that transient receptor potential canonical 3 (TRPC3), a key regulator of atherosclerosis development, was the direct target of miR-454-3p. Furthermore, TRPC3 overexpression abolished the anti-apoptotic effect of miR-454-3p on HAECs. These results revealed a novel role of miR-454-3p in ox-LDL-induced apoptosis in HAECs.
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Registered trials
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