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

By Eva van Rooij, L. Sutherland, J. Thatcher, J. Dimaio, R. Naseem, W. Marshall, Joseph A. Hill, E. Olson. Proceedings of the National Academy of Sciences of the United States of America, 2008

1,881 citations recorded by the source corpus.

Subfields: Cancer Research, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/b0df167ea12b73a8881d4506716cb521e9439cf8

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Citations in the corpus

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).”
Modulation of K-ras-dependent lung tumorigenesis by microRNA-21 (2010, positive): “…in expected Mendelian ratios. miR-21 expression increases in mouse models of cardiac hypertrophy and following myocardial infarction; however, adult male CAG-miR-21 mice showed no signs of heart failure compared to littermate controls (Fig- ure S1E) (van Rooij et al., 2006; van Rooij et al., 2008).”
MicroRNAs in stress signaling and human disease (2012, background): “…(Hill and Olson, 2008). miR-29 is downregulated under conditions of cardiovascular disease associated with fibrosis and excessive ECM production (Boon et al., 2011; Cushing et al., 2011; van Rooij et al., 2008), implicating this miRNA as a repressive mediator of fibrotic disease (Figure 3A).”
Recent developments in myofibroblast biology: paradigms for connective tissue remodeling. (2012, background): “Down-regulation of miR-29 in cardiac fibroblasts in vitro and in vivo induces fibrosis-associated genes, whereas its overexpression has a fibrosis-suppressing effect.(46) A comparable fibrosis-suppressing role has been demonstrated for miR-200a in the kidney(49) and liver.”