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Eva van Rooij

Researcher at Utrecht University

Publications -  86
Citations -  15486

Eva van Rooij is an academic researcher from Utrecht University. The author has contributed to research in topics: Heart failure & Gene expression. The author has an hindex of 39, co-authored 74 publications receiving 14287 citations. Previous affiliations of Eva van Rooij include University of Texas Southwestern Medical Center & Royal Netherlands Academy of Arts and Sciences.

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

TL;DR: It is concluded that miR-29 acts as a regulator of cardiac fibrosis and represents a potential therapeutic target for tissue fibrosis in general.
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Control of Stress-Dependent Cardiac Growth and Gene Expression by a MicroRNA

TL;DR: It is found that a cardiac-specific microRNA (miR-208) encoded by an intron of the αMHC gene is required for cardiomyocyte hypertrophy, fibrosis, and expression of βMHC in response to stress and hypothyroidism.
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A signature pattern of stress-responsive microRNAs that can evoke cardiac hypertrophy and heart failure

TL;DR: Findings reveal an important role for specific miRNAs in the control of hypertrophic growth and chamber remodeling of the heart in response to pathological signaling and point to mi RNAs as potential therapeutic targets in heart disease.
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A Family of microRNAs Encoded by Myosin Genes Governs Myosin Expression and Muscle Performance

TL;DR: Findings reveal that myosin genes not only encode the major contractile proteins of muscle, but act more broadly to influence muscle function by encoding a network of intronic miRNAs that control muscle gene expression and performance.
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Modulation of K-Ras-Dependent Lung Tumorigenesis by MicroRNA-21

TL;DR: It is shown that overexpression of miR-21 enhances tumorigenesis and that genetic deletion of mi R-21 partially protects against tumor formation, and that overexpression of miRs drives tumorigenisation through inhibition of negative regulators of the Ras/MEK/ERK pathway and inhibition of apoptosis.