ArticleJournal of physiology and biochemistry2016
MicroRNA-9 regulates cardiac fibrosis by targeting PDGFR-β in rats.
Article in Journal of physiology and biochemistry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 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
14 citing papers in PubMed, 33 citations in OpenAlex.
- Emerging roles of non-coding RNAs in fibroblast to myofibroblast transition and fibrotic diseases.Frontiers in pharmacology · 2024Review
- Integrated bioinformatics analysis for identifying key genes and pathways in female and male patients with dilated cardiomyopathy.Scientific reports · 2023Article
- MicroRNA-9 rescues hyperglycemia-induced endothelial cell dysfunction and promotes arteriogenesis through downregulating Notch1 signaling.Molecular and cellular biochemistry · 2021Article
- Small proline-rich repeat 3 is a novel coordinator of PDGFRβ and integrin β1 crosstalk to augment proliferation and matrix synthesis by cardiac fibroblasts.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020Article
- Decrypting the crosstalk of noncoding RNAs in the progression of IPF.Molecular biology reports · 2020Review
- Construction and Analysis of a ceRNA Network in Cardiac Fibroblast During Fibrosis Based onFrontiers in genetics · 2020Article
- MiR-32-5p influences high glucose-induced cardiac fibroblast proliferation and phenotypic alteration by inhibiting DUSP1.BMC molecular biology · 2019Article
- Potential regulatory role of circular RNA in idiopathic pulmonary fibrosis.International journal of molecular medicine · 2018Article
- MiR-33 promotes myocardial fibrosis by inhibiting MMP16 and stimulating p38 MAPK signaling.Oncotarget · 2018Article
- MicroRNA-1291 promotes endometrial fibrosis by regulating the ArhGAP29-RhoA/ROCK1 signaling pathway in a murine model.Molecular medicine reports · 2017Article
- MicroRNA-98 inhibits TGF-β1-induced differentiation and collagen production of cardiac fibroblasts by targeting TGFBR1.Human cell · 2017Article
- Effect of ALDH2 on High Glucose-Induced Cardiac Fibroblast Oxidative Stress, Apoptosis, and Fibrosis.Oxidative medicine and cellular longevity · 2017Article
- Circulating exosome microRNA associated with heart failure secondary to myxomatous mitral valve disease in a naturally occurring canine model.Journal of extracellular vesicles · 2017Article
- MicroRNA-9 inhibits high glucose-induced proliferation, differentiation and collagen accumulation of cardiac fibroblasts by down-regulation of TGFBR2.Bioscience reports · 2016Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The proliferation of cardiac fibroblasts (CFs) and excessive deposition of extracellular matrix (ECM) are the main pathological characteristics of cardiac fibrosis. In recent years, microRNAs (miRNAs) have been found to be a new kind of regulator in cardiac fibrosis. The purpose of this study was to investigate the role of microRNA-9 (miR-9) in the process of cardiac fibrosis and its mechanism. Treatment of cultured neonatal rat CFs with PDGF-BB or serum suppressed the expression of miR-9. Overexpression of miR-9 obviously inhibited neonatal rat CFs proliferation and collagen production as detected by MTT assays, qRT-PCR, and western blotting. The effects of miR-9 in CFs were abrogated by co-transfection with miR-9 inhibitors. Overexpression of miR-9 reduced the mRNA and protein levels of PDGFR-βand its downstream protein, extracellular signal-regulated kinase (ERK) 1/2. Silencing PDGFR-βby small interfering RNA mimicked the anti-fibrotic action of miR-9, whereas overexpression of PGDFR-β canceled the effect of miR-9 in cultured CFs. Dual-luciferase reporter assays showed that PDGFR-βwas a direct target of miR-9. Overexpression of miR-9 inhibited cardiac fibrosis by targeting PDGFR-β, indicating that miR-9 might play a role in the treatment of cardiac fibrosis.
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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.