ArticleAnnals of thoracic and cardiovascular surgery : official journal of the Association of Thoracic and Cardiovascular Surgeons of Asia2020
MiR-26b Suppresses the Development of Stanford Type A Aortic Dissection by Regulating HMGA2 and TGF-β/Smad3 Signaling Pathway.
Article in Annals of thoracic and cardiovascular surgery : official journal of the Association of Thoracic and Cardiovascular Surgeons of Asia, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.
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Who cites it
18 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Diagnostic biomarkers and aortic dissection: a systematic review and meta-analysis.BMC cardiovascular disorders · 2023Pooled it
- Mitochondrial cardiovascular diseases: molecular mechanisms, multi-omics exploration and therapeutic strategies.Journal of advanced research · 2026Review
- LXRα Promotes Abdominal Aortic Aneurysm Formation Through UHRF1 Epigenetic Modification of miR-26b-3p.Circulation · 2024Article
- High glucose promotes atherosclerosis by regulating miRNA let7d-5p level.Journal of diabetes investigation · 2024Article
- LncRNA HCG18 affects aortic dissection through the miR-103a-3p/HMGA2 axis by modulating proliferation and apoptosis of vascular smoothing muscle cells.Clinics (Sao Paulo, Brazil) · 2024Article
- LINC02015 modulates the cell proliferation and apoptosis of aortic vascular smooth muscle cells by transcriptional regulation and protein interaction network.Cell death discovery · 2023Article
- MicroRNA regulation of phenotypic transformations in vascular smooth muscle: relevance to vascular remodeling.Cellular and molecular life sciences : CMLS · 2023Review
- Potential biomarkers of aortic dissection based on expression network analysis.BMC cardiovascular disorders · 2023Article
- Emerging Role of Non-Coding RNAs in Aortic Dissection.Biomolecules · 2022Review
- The role of vascular smooth muscle cells in the development of aortic aneurysms and dissections.European journal of clinical investigation · 2022Review
- Long non-coding RNA HIF1A-AS2 modulates the proliferation, migration, and phenotypic switch of aortic smooth muscle cells in aortic dissection via sponging microRNA-33b.Bioengineered · 2022Article
- Non-coding RNAs Regulate the Pathogenesis of Aortic Dissection.Frontiers in cardiovascular medicine · 2022Review
- Identification of pathological-related and diagnostic potential circular RNAs in Stanford type A aortic dissection.Frontiers in cardiovascular medicine · 2022Article
- Association of TGF-β Canonical Signaling-Related Core Genes With Aortic Aneurysms and Aortic Dissections.Frontiers in pharmacology · 2022Review
- Risk factors of continuous renal replacement therapy following total aortic arch replacement under moderate hypothermia.Annals of translational medicine · 2021Article
- SHED aggregate exosomes shuttled miR-26a promote angiogenesis in pulp regeneration via TGF-β/SMAD2/3 signalling.Cell proliferation · 2021Article
- Article
- Non-coding RNAs in aortic dissection: From biomarkers to therapeutic targets.Journal of cellular and molecular medicine · 2020Review
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeStanford type A aortic dissection (TAAD) is one of the most dangerous cardiovascular diseases. MicroRNAs (miRNAs) have been considered as potential therapeutic targets for TAAD. In this present study, we aimed to investigate the functional role and regulatory mechanism of miR-26b in TAAD development. MATERIALS AND
methodsMiR-26b mRNA expression was detected by real-time polymerase chain reaction (RT-PCR) and protein levels were measured by Western blot. Verifying the direct target of miR-26b was used by dual luciferase assay, RT-PCR, and Western blot. Cell Counting Kit-8 (CCK-8) and TUNEL staining assays were applied for detecting rat aortic vascular smooth muscle cells (VSMCs) viability and apoptosis, respectively.
resultsWe found that miR-26b was under-expressed in TAAD patients and closely associated with the poor prognosis of TAAD patients. Re-expression of miR-26b facilitated while knockdown of miR-26b inhibited VSMC proliferation. However, miR-26b showed the opposite effect on cell apoptosis. More importantly, high-mobility group AT-hook 2 (HMGA2) was verified as the direct target of miR-26b. Furthermore, transforming growth factor beta (TGF-β)/Smad3 signaling pathway was involved in the development of TAAD modulated by miR-26b.
conclusionmiR-26b impeded TAAD development by regulating HMGA2 and TGF-β/Smad3 signaling pathway, which provided a potential biomarker for TAAD treatment.
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