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

By Sashwati Roy, S. Khanna, S. Hussain, S. Biswas, A. Azad, Cameron Rink, S. Gnyawali, S. Shilo, G. Nuovo, Chandan K. Sen. Cardiovascular Research, 2009

646 citations recorded by the source corpus.

Subfields: Cancer Research, Cardiology and Cardiovascular Medicine

View Paper: https://www.semanticscholar.org/paper/113aff430d94be720536dc240a40c1a895d1ebc9

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In Cancer Research

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Citations in the corpus

Non-coding RNAs in Development and Disease: Background, Mechanisms, and Therapeutic Approaches. (2016, background): “Later on, other studies have shown that miR-21 has also an impact on expression of MMP2 and TGF- receptor type III, thus acting on multiple pro-fibrotic pathways (163, 232).”
MicroRNAs in development and disease. (2011, background): “In these cells, it inhibits PTEN and induces upregulation of metalloprotease-2 (515), which promotes fibrosis.”
miR-21 mediates fibrogenic activation of pulmonary fibroblasts and lung fibrosis (2010, background): “In experimental models of myocardial infarction, phosphatase and tensin homologue (PTEN) was down-regulated by miR-21 in cardiofibroblasts from the infracted areas (Roy et al., 2009).”
Ischemia/Reperfusion (2016, neutral): “tion involved in cardiac cell death, arrhythmogenesis, fibrosis and extracellular matrix remodeling, and angiogenesis (276, 296, 388, 674, 858, 894).”
Cell Biology of Ischemia/Reperfusion Injury (2012, result): “Similar findings were obtained in the heart (Roy et al., 2009), hippocampus (Yuan et al., 2010), skeletal muscle (Greco et al., 2009), kidney (Godwin et al., 2010), and liver (Xu et al., 2009).”