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

By Thomas Thum, C. Gross, J. Fiedler, T. Fischer, S. Kissler, Markus Bussen, P. Galuppo, S. Just, W. Rottbauer, S. Frantz and 13 more. Nature, 2008

2,432 citations recorded by the source corpus.

Subfields: Cancer Research, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/8f21c13557ea2a64b4e6de050241dd255c22e9ad

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Citations in the corpus

MicroRNAs in development and disease. (2011, background): “While miR-21 is upregulated in the whole heart during pathological hypertrophy, it appears that its increase in the myofibroblasts is more significant than it is in the myocytes (612).”
Transcriptional Regulation and its Misregulation in Disease (2013, positive): “…disease, including arrhythmia, fibrosis, hypertrophy due to high pressure and misregulation of cardiac energy metabolism (Callis et al., 2009; Care et al., 2007; Grueter et al., 2012; Luo et al., 2008; Thum et al., 2008; van Rooij et al., 2007; van Rooij et al., 2008; Yang et al., 2007).”
MicroRNA expression in response to murine myocardial infarction: miR-21 regulates fibroblast metalloprotease-2 via phosphatase and tensin homologue. (2009, positive): “While this work was in review, two other publications have recognized the significance of miR-21 in the heart.(34,35) Changes in miR-21, specifically in CFs, can regulate heart failure.”
Non-coding RNAs in disease: from mechanisms to therapeutics (2023, positive): “Silencing of miR-21 via antagomir-21 could disrupt cardiac allograft vasculopathy and prolong cardiac allograft survival 137 as well as reduce hypertrophy and fibrosis and restore impaired cardiac function 139 .”
miR-21 mediates fibrogenic activation of pulmonary fibroblasts and lung fibrosis (2010, background): “Aberrant expression of miRNAs is closely associated with initiation and progression of pathophysiologic processes including diabetes, cancer, and cardiovascular disease (Thum et al., 2008; Croce, 2009; Latronico and Condorelli, 2009; Pandey et al., 2009).”
MicroRNA profiling of multiple sclerosis lesions identifies modulators of the regulatory protein CD47. (2009, background): “Although the quantitative impact of miRNA ‘fine tuning’ on gene expression levels is relatively small, miRNAs are nevertheless implicated in the pathogenesis of different diseases, including cancer, cardiac failure and neurodegenerative diseases (Papagiannakopoulos and Kosik, 2008; Thum et al., 2008”
Matrix as an Interstitial Transport System (2014, background): “MiR-21 is elevated in pressure overload(142) and ischemic cardiomyopathy(143) and reported to trigger myocardial fibrosis because its silencing prevented fibrosis in pressure overloaded cardiomyopathy.(142) Consistently, miR-21–deficient mice were protected against renal injury and fibrosis.”
Cardiac fibroblast-derived microRNA passenger strand-enriched exosomes mediate cardiomyocyte hypertrophy. (2014, neutral): “We previously showed, by in vitro and in vivo experiments, that miR-21 has no significant effect in cardiomyocyte hypertrophy (17).”