A signature pattern of stress-responsive microRNAs that can evoke cardiac hypertrophy and heart failure

By Eva van Rooij, L. Sutherland, Ning Liu, Andrew H. Williams, John R. McAnally, R. Gerard, J. Richardson, E. Olson. Proceedings of the National Academy of Sciences of the United States of America, 2006

1,550 citations recorded by the source corpus.

Subfields: Cancer Research, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/b60fcca43f122e24b9e5ac8149b46944a46fd5b3

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Citations in the corpus

Non-coding RNAs in human disease (2011, background): “Furthermore, myocardial tissue from heart failure patients has a distinct miRNA expression profile as compared to a healthy myocardiu”
Altered microRNA expression in human heart disease. (2007, background): “Upregulation of miR-214 may contribute to cardiac hypertrophy, as cardiomyocyte overexpression of miR-214 induced cardiomyocyte hypertrophy (19).”
microRNA as Biomarkers and Diagnostics (2016, background): “…are deregulated in viral infections (Lecellier et al., 2005), nervous system disorders (Mehler and Mattick, 2007), cardiovascular disorders (van Rooij et al., 2006a; Hebert and De Strooper, 2009; Ai et al., 2010; Wang et al., 2010), muscular disorders (Eisenberg et al., 2007), diabetes, and…”
A family of microRNAs encoded by myosin genes governs myosin expression and muscle performance. (2009, methodology): “Northern blots to detect miRNAs were performed as described previously ( van Rooij et al., 2006 ).”
MicroRNA-208a is a regulator of cardiac hypertrophy and conduction in mice. (2009, background): “In addition, miRNA expression profiling studies demonstrate that the expression of specific miRNAs changes in diseased human hearts, pointing to the involvement of miRNAs in cardiomyopathies (15, 16).”
Dysregulation of cardiogenesis, cardiac conduction, and cell cycle in mice lacking miRNA-1-2. (2007, background): “Although significant dysregulation of miRNA expression has been reported in cardiac disease (Sayed et al., 2007; van Rooij et al., 2006), it remains unknown if the heart requires miRNA function for normal development or maintenance.”
The muscle-specific microRNA miR-1 regulates cardiac arrhythmogenic potential by targeting GJA1 and KCNJ2 (2011, result): “However, an earlier study in which the same model and approach were used failed to observe reduction of miR-1 (ref”
The Expression of MicroRNA miR-107 Decreases Early in Alzheimer's Disease and May Accelerate Disease Progression through Regulation of β-Site Amyloid Precursor Protein-Cleaving Enzyme 1 (2008, background): “BACE1 cleaves the -amyloid precursor protein creating the neurotoxic -amyloid peptide A 1– 42 (Vassar et al., 1999; Haniu et al., 2000).”
MicroRNA expression in response to murine myocardial infarction: miR-21 regulates fibroblast metalloprotease-2 via phosphatase and tensin homologue. (2009, neutral): “The first expression profiling of miR in the heart was reported only recently.(21) These studies aimed at examining heart failure and cardiac hypertrophy.”
Dysregulation of microRNAs after myocardial infarction reveals a role of miR-29 in cardiac fibrosis (2008, background): “Members of the miR-29 family are also down-regulated in response to pressure overload and chronic calcineurin signaling (9), pathological stimuli also associated with cardiac fibrosis.”