ArticlePloS one2015
Sp1 Mediates a Therapeutic Role of MiR-7a/b in Angiotensin II-Induced Cardiac Fibrosis via Mechanism Involving the TGF-β and MAPKs Pathways in Cardiac Fibroblasts.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 32 citations in OpenAlex.
- Role of Specificity Protein 1 (SP1) in Cardiovascular Diseases: Pathological Mechanisms and Therapeutic Potentials.Biomolecules · 2024Review
- P21‑activated kinase 1 mediates angiotensin II‑induced differentiation of human atrial fibroblasts via the JNK/c‑Jun pathway.Molecular medicine reports · 2021Article
- MicroRNAs in Transforming Growth Factor-Beta Signaling Pathway Associated With Fibrosis Involving Different Systems of the Human Body.Frontiers in molecular biosciences · 2021Review
- The effects of the Xijiao Dihuang decoction combined with Yinqiao powder on miRNA-mRNA profiles in mice infected with influenza a virus.BMC complementary medicine and therapies · 2020Article
- Morphological and Functional Characteristics of Animal Models of Myocardial Fibrosis Induced by Pressure Overload.International journal of hypertension · 2020Review
- Inhibition ofJournal of cardiovascular development and disease · 2019Article
- UFL1 promotes histone H4 ufmylation and ATM activation.Nature communications · 2019Article
- Effects of AT1 receptor antagonism on interstitial and ultrastructural remodeling of heart in response to a hypercaloric diet.Physiological reports · 2019Article
- Salvianolic Acid B-Alleviated Angiotensin II Induces Cardiac Fibrosis by Suppressing NF-κB Pathway In Vitro.Medical science monitor : international medical journal of experimental and clinical research · 2018Article
- Article
- Matrine suppresses cardiac fibrosis by inhibiting the TGF‑β/Smad pathway in experimental diabetic cardiomyopathy.Molecular medicine reports · 2018Article
- Comparison of Cardiac miRNA Transcriptomes Induced by Diabetes and Rapamycin Treatment and Identification of a Rapamycin-Associated Cardiac MicroRNA Signature.Oxidative medicine and cellular longevity · 2018Article
- Article
- T3 peptide, a fragment of tumstatin, stimulates proliferation and migration of cardiac fibroblasts through activation of Akt signaling pathway.Naunyn-Schmiedeberg's archives of pharmacology · 2017Article
- Article
- MiR-590 Promotes Transdifferentiation of Porcine and Human Fibroblasts Toward a Cardiomyocyte-Like Fate by Directly Repressing Specificity Protein 1.Journal of the American Heart Association · 2016Article
- MicroRNA-142-3p inhibits hypoxia/reoxygenation‑induced apoptosis and fibrosis of cardiomyocytes by targeting high mobility group box 1.International journal of molecular medicine · 2016Article
- miR-7a/b attenuates post-myocardial infarction remodeling and protects H9c2 cardiomyoblast against hypoxia-induced apoptosis involving Sp1 and PARP-1.Scientific reports · 2016Article
- MicroRNA: A new therapeutic strategy for cardiovascular diseases.Trends in cardiovascular medicine · 2016Review
- microRNA-7-5p inhibits melanoma cell proliferation and metastasis by suppressing RelA/NF-κB.Oncotarget · 2016Article
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
MicroRNA-7a/b (miR-7a/b) protects cardiac myocytes from apoptosis during ischemia/reperfusion injury; however, its role in angiotensin II (ANG II)-stimulated cardiac fibroblasts (CFs) remains unknown. Therefore, the present study investigated the anti-fibrotic mechanism of miR-7a/b in ANG II-treated CFs. ANG II stimulated the expression of specific protein 1 (Sp1) and collagen I in a dose- and time-dependent manner, and the overexpression of miR-7a/b significantly down-regulated the expression of Sp1 and collagen I stimulated by ANG II (100 nM) for 24 h. miR-7a/b overexpression effectively inhibited MMP-2 expression/activity and MMP-9 expression, as well as CF proliferation and migration. In addition, miR-7a/b also repressed the activation of TGF-β, ERK, JNK and p38 by ANG II. The inhibition of Sp1 binding activity by mithramycin prevented collagen I overproduction; however, miR-7a/b down-regulation reversed this effect. Further studies revealed that Sp1 also mediated miR-7a/b-regulated MMP expression and CF migration, as well as TGF-β and ERK activation. In conclusion, miR-7a/b has an anti-fibrotic role in ANG II-treated CFs that is mediated by Sp1 mechanism involving the TGF-β and MAPKs pathways.
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