miR-21 and cardiac fibrosis: another brick in the wall?: Figure 1

Anti–microRNA-21 oligonucleotides prevent Alport nephropathy progression by stimulating metabolic pathways

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Fibrosis: ultimate and proximate causes

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microRNAs in Cardiovascular Diseases

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MicroRNA-29 family, a crucial therapeutic target for fibrosis diseases

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Extracellular Matrix Secretion by Cardiac Fibroblasts

(2013) Mélanie Abonnenc et al.   CIRCULATION RESEARCH

Circulating miR-29a, Among Other Up-Regulated MicroRNAs, Is the Only Biomarker for Both Hypertrophy and Fibrosis in Patients With Hypertrophic Cardiomyopathy

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A novel reciprocal loop between microRNA-21 and TGFβRIII is involved in cardiac fibrosis

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Mechanisms of fibrosis: therapeutic translation for fibrotic disease

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Transforming Growth Factor-β–Induced Endothelial-to-Mesenchymal Transition Is Partly Mediated by MicroRNA-21

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MiR-133a regulates collagen 1A1: Potential role of miR-133a in myocardial fibrosis in angiotensin II-dependent hypertension

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The microRNA miR-29 controls innate and adaptive immune responses to intracellular bacterial infection by targeting interferon-γ

(2011) Feng Ma et al.   NATURE IMMUNOLOGY

Stress-dependent cardiac remodeling occurs in the absence of microRNA-21 in mice

(2010) David M. Patrick et al.   JOURNAL OF CLINICAL INVESTIGATION

MicroRNA expression in response to murine myocardial infarction: miR-21 regulates fibroblast metalloprotease-2 via phosphatase and tensin homologue

(2009) Sashwati Roy et al.   CARDIOVASCULAR RESEARCH

miR-133 and miR-30 Regulate Connective Tissue Growth Factor

(2008) Rudy F. Duisters et al.   CIRCULATION RESEARCH

MicroRNA-21 contributes to myocardial disease by stimulating MAP kinase signalling in fibroblasts

(2008) Thomas Thum et al.   NATURE

Dysregulation of microRNAs after myocardial infarction reveals a role of miR-29 in cardiac fibrosis

(2008) E. van Rooij et al.   PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA