ArticleBioscience reports2020
miR-29b-3p inhibits post-infarct cardiac fibrosis by targeting FOS.
Article in Bioscience reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 39 citations in OpenAlex.
- Myeloid infiltration and epidermal dysregulation characterize cutaneous photosensitivity in systemic lupus erythematosus.Science translational medicine · 2026Article
- Integrated miRNA-cytokine profiling reveals a molecular signature of cachexia in patients with chronic heart failure.ESC heart failure · 2026Article
- Decoding noncoding RNAs in regulating cardiovascular aging and age-related conditions: the emerging landscape.Science China. Life sciences · 2026Review
- Epigenetic Regulation and Molecular Mechanisms in Cardiovascular Diseases: A Review of Recent Advances and Therapeutic Implications.International journal of molecular sciences · 2026Review
- Impact of microRNAs on cardiovascular diseases and aging.The Journal of international medical research · 2024Review
- An overview of CCN4 (WISP1) role in human diseases.Journal of translational medicine · 2024Review
- miR-29b-3p regulates cardiomyocytes pyroptosis in CVB3-induced myocarditis through targeting DNMT3A.Cellular & molecular biology letters · 2024Article
- Identification of genetic associations between acute myocardial infarction and non-small cell lung cancer.Frontiers in molecular biosciences · 2024Article
- Predictive Value of Serum microRNA-29b-3p in Recurrence of Atrial Fibrillation After Radiofrequency Catheter Ablation.Clinical interventions in aging · 2024Article
- Article
- Dihydroartemisinin inhibits the activation and proliferation of hepatic stellate cells by regulating miR‑29b‑3p.International journal of molecular medicine · 2023Article
- The Role of ncRNAs in Cardiac Infarction and Regeneration.Journal of cardiovascular development and disease · 2023Review
- Identification of diagnostic immune-related gene biomarkers for predicting heart failure after acute myocardial infarction.Open medicine (Warsaw, Poland) · 2023Article
- Post-myocardial infarction fibrosis: Pathophysiology, examination, and intervention.Frontiers in pharmacology · 2023Review
- Based on network pharmacology and in vitro experiments to prove the effective inhibition of myocardial fibrosis by Buyang Huanwu decoction.Bioengineered · 2022Article
- MSCs-Derived Extracellular Vesicles Carrying miR-212-5p Alleviate Myocardial Infarction-Induced Cardiac Fibrosis via NLRC5/VEGF/TGF-β1/SMAD Axis.Journal of cardiovascular translational research · 2022Article
- Roles of exosomes and exosome-derived miRNAs in pulmonary fibrosis.Frontiers in pharmacology · 2022Review
- Overexpression of ring finger protein 20 inhibits the progression of liver fibrosis via mediation of histone H2B lysine 120 ubiquitination.Human cell · 2021Article
- Targeting Epigenetics and Non-coding RNAs in Myocardial Infarction: From Mechanisms to Therapeutics.Frontiers in genetics · 2021Review
- Overexpression of MiR-29b-3p Inhibits Atrial Remodeling in Rats by Targeting PDGF-B Signaling Pathway.Oxidative medicine and cellular longevity · 2021Article
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
backgroundCardiac fibrosis after myocardial infarction (MI) is a major cause of heart deterioration. Recently, the roles of microRNAs (miRNAs) in various cardiovascular diseases associated with cardiac fibrosis have been extensively investigated. The present study aimed to investigate the role and mechanism of miR-29b-3p in cardiac fibrosis after MI.
methodsmiR-29b-3p expression in TGF-β1-activated cardiac fibroblasts (CFs) was detected by qRT-PCR. Cell Counting Kit-8 (CCK-8) and Trans-well assays were performed to evaluate CFs proliferation and migration ability, respectively. Protein expressions of α-SMA, collagen I, collagen III, MMP2, and MMP9 were examined by Western blot assay. Bioinformatics, luciferase, and RNA immunoprecipitation (RIP) assays were carried out to determine whether FOS was targeted by miR-29b-3p.
resultsTGF-β1 treatment dose-dependently curbed miR-29b-3p expression in CFs. miR-29b-3p restrained the promotive impacts of TGF-β1 on CFs proliferation, migration, and differentiation. FOS was affirmed to be a target of miR-29b-3p, elevated expression of FOS reversed the inhibitory effects of miR-29b-3p on cell proliferation, migration, and differentiation in TGF-β1-activated CFs.
conclusionmiR-29b-3p degraded the pro-fibrosis effect induced by TGF-β1 via targeting FOS, providing a prospective therapeutic avenue for cardiac fibrosis after MI.
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