ArticleJournal of molecular and cellular cardiology2013
Angiotensin II stimulates cardiac fibroblast migration via the differential regulation of matrixins and RECK.
Article in Journal of molecular and cellular cardiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers.
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Who cites it
67 citing papers in PubMed.
- LncRNA SNHG8 contributes to post-myocardial infarction cardiac fibrosis and is functionally associated with miR-192-3p.Journal of molecular histology · 2026Article
- Bromodomain-containing protein 4 in inflammatory diseases: molecular mechanisms and therapeutic potential.Journal of inflammation (London, England) · 2026Review
- The Roles of the Membrane-Anchored Glycoprotein RECK in Animal Development, Tumor Suppression, and Beyond.Life (Basel, Switzerland) · 2026Review
- Unraveling the interplay between RAS axes and NOX signaling in fibroblasts during cardiac fibrosis.Molecular and cellular biochemistry · 2026Review
- Review
- Loss of hepatocyte-specific RECK exacerbates metabolic dysfunction-associated steatohepatitis.American journal of physiology. Endocrinology and metabolism · 2025Article
- The Dual Role of NOX4 in Cardiovascular Diseases: Driver of Oxidative Stress and Mediator of Adaptive Remodeling.Antioxidants (Basel, Switzerland) · 2025Review
- Beneficial Effects of Chymase Inhibition on Cardiac Diastolic Function and Remodeling Induced by Chronic Angiotensin II Stimulation.International journal of molecular sciences · 2025Article
- RECK as a Potential Crucial Molecule for the Targeted Treatment of Sepsis.Journal of inflammation research · 2025Review
- Article
- Morroniside improves AngII-induced cardiac fibroblast proliferation, migration, and extracellular matrix deposition by blocking p38/JNK signaling pathway through the downregulation of KLF5.Naunyn-Schmiedeberg's archives of pharmacology · 2024Article
- Fibroblast-specific PRMT5 deficiency suppresses cardiac fibrosis and left ventricular dysfunction in male mice.Nature communications · 2024Article
- The lipolysis inhibitor acipimox reverses the cardiac phenotype induced by electronic cigarettes.Scientific reports · 2023Article
- NKRF in Cardiac Fibroblasts Protects against Cardiac Remodeling Post-Myocardial Infarction via Human Antigen R.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- Bidirectional negative feedback actions of DNMT3A and miR-145 in regulating autophagy in cardiac fibroblasts and affecting myocardial fibrosis.Journal of bioenergetics and biomembranes · 2023Article
- Extracellular matrix remodelling in obesity and metabolic disorders.Life metabolism · 2023Article
- Cardiovascular manifestations of inflammatory bowel diseases and the underlying pathogenic mechanisms.American journal of physiology. Regulatory, integrative and comparative physiology · 2023Review
- Empagliflozin Reverses Oxidized LDL-Induced RECK Suppression, Cardiotrophin-1 Expression, MMP Activation, and Human Aortic Smooth Muscle Cell Proliferation and Migration.Mediators of inflammation · 2023Article
- Myofibroblast specific targeting approaches to improve fibrosis treatment.Chemical communications (Cambridge, England) · 2022Review
- Intercellular transfer of miR-200c-3p impairs the angiogenic capacity of cardiac endothelial cells.Molecular therapy : the journal of the American Society of Gene Therapy · 2022Article
7 more citing papers are in PubMed but not listed here.
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Authors and funding
9 authors.
Funding
Abstract
Sustained induction and activation of matrixins (matrix metalloproteinases or MMPs), and the destruction and deposition of extracellular matrix (ECM), are the hallmarks of cardiac fibrosis. The reversion-inducing-cysteine-rich protein with Kazal motifs (RECK) is a unique membrane-anchored endogenous MMP regulator. We hypothesized that elevated angiotensin II (Ang II), which is associated with fibrosis in the heart, differentially regulates MMPs and RECK both in vivo and in vitro. Continuous infusion of Ang II into male C57Bl/6 mice for 2weeks resulted in cardiac fibrosis, with increased expressions of MMPs 2, 7, 9 and 14, and of collagens Ia1 and IIIa1. The expression of RECK, however, was markedly suppressed. These effects were inhibited by co-treatment with the Ang II type 1 receptor (AT1) antagonist losartan. In vitro, Ang II suppressed RECK expression in adult mouse cardiac fibroblasts (CF) via AT1/Nox4-dependent ERK/Sp1 activation, but induced MMPs 2, 14 and 9 via NF-κB, AP-1 and/or Sp1 activation. Further, while forced expression of RECK inhibits, its knockdown potentiates Ang II-induced CF migration. Notably, RECK overexpression reduced Ang II-induced MMPs 2, 9 and 14 activation, but enhanced collagens Ia1 and IIIa1 expression and soluble collagen release. These results demonstrate for the first time that Ang II suppresses RECK, but induces MMPs both in vivo and in vitro, and RECK overexpression blunts Ang II-induced MMP activation and CF migration in vitro. Strategies that upregulate RECK expression in vivo have the potential to attenuate sustained MMP expression, and blunt fibrosis and adverse remodeling in hypertensive heart diseases.
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