ArticleBioengineered2022
MiR-410-3p facilitates Angiotensin II-induced cardiac hypertrophy by targeting Smad7.
Article in Bioengineered, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- Vascular endothelial cell-derived small extracellular vesicles: A protective role against cardiomyocyte apoptosis in ischemia-reperfusion injury through miR410-3p-modulatedThe Journal of international medical research · 2026Article
- Epigenetic Mechanisms in Heart Diseases.Reviews in cardiovascular medicine · 2025Review
- Microrna363-5p targets thrombospondin3 to regulate pathological cardiac remodeling.Molecular and cellular biochemistry · 2025Article
- Screening and validation of key microRNAs regulating muscle development in Hanper sheep.PloS one · 2025Article
- Cardiovascular Disease and miRNAs: Possible Oxidative Stress-Regulating Roles of miRNAs.Antioxidants (Basel, Switzerland) · 2024Review
- Noncoding RNAs as Key Regulators for Cardiac Development and Cardiovascular Diseases.Journal of cardiovascular development and disease · 2023Review
- 4'‑O‑methylbavachalcone inhibits succinate induced cardiomyocyte hypertrophy via the NFATc4 pathway.Experimental and therapeutic medicine · 2023Article
- Bone mesenchymal stem cells (BMSCs)-derived exosomal microRNA-21-5p regulates Kruppel-like factor 3 (KLF3) to promote osteoblast proliferationBioengineered · 2022Article
- MicroRNA-122-3p plays as the target of long non-coding RNA LINC00665 in repressing the progress of arthritis.Bioengineered · 2022Article
- miR-125a attenuates the malignant biological behaviors of cervical squamous cell carcinoma cells through Rad51.Bioengineered · 2022Article
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
MicroRNAs (miRNAs) have emerged as important regulators in the development of cardiovascular diseases. miR-410-3p was shown to play a protective or detrimental role in the progression in cardiovascular events. However, the exact role and the underlying mechanism of miR-410-3p in cardiac hypertrophy have not been documented. The current work was aimed to determine the role and underlying mechanism of miR-410-3p on Angiotensin II (Ang II) induced cardiac hypertrophy. FITC-phalloidin staining was used for determination of cardiomyocyte surface area. Quantitative reverse transcription polymerase chain reaction (qRT-PCR) was performed to identify mRNA expression level of hypertrophic markers. Smad7 protein expression level was analyzed using Western blot. Dual-luciferase reporter assay was used to examine the regulatory function of miR-410-3p on Smad7. MiR-410-3p was found significantly up-regulated in Ang II-induced cardiac hypertrophy. MiR-410-3p inhibitor remarkably alleviated cardiomyocyte hypertrophic changes. Dual-luciferase reporter assay result indicated that miR-410-3p directly targeted Smad7 and miR-410-3p inhibitor effectively prevented Ang II triggered down-regulation of Smad7. Moreover, Smad7 overexpression significantly reversed the pro-hypertrophic effect of miR-410-3p. In summary, our findings revealed that miR-410-3p mediated Ang II-induced cardiac hypertrophy via targeting inhibition of Smad7.
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