An Analysis of the Global Expression of MicroRNAs in an Experimental Model of Physiological Left Ventricular Hypertrophy

MicroRNA-150 aggravates H2O2-induced cardiac myocyte injury by down-regulating c-myb gene

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Cardiac-Specific Over-Expression of Epidermal Growth Factor Receptor 2 (ErbB2) Induces Pro-Survival Pathways and Hypertrophic Cardiomyopathy in Mice

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MicroRNA-27a/b controls endothelial cell repulsion and angiogenesis by targeting semaphorin 6A

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MicroRNA-195 promotes palmitate-induced apoptosis in cardiomyocytes by down-regulating Sirt1

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Aerobic Exercise Training–Induced Left Ventricular Hypertrophy Involves Regulatory MicroRNAs, Decreased Angiotensin-Converting Enzyme-Angiotensin II, and Synergistic Regulation of Angiotensin-Converting Enzyme 2-Angiotensin (1-7)

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MiR-150 promotes gastric cancer proliferation by negatively regulating the pro-apoptotic gene EGR2

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Ischaemic preconditioning-regulated miR-21 protects heart against ischaemia/reperfusion injury via anti-apoptosis through its target PDCD4

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Assessment of Plasma miRNAs in Congestive Heart Failure

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Circulating MicroRNA-208b and MicroRNA-499 Reflect Myocardial Damage in Cardiovascular Disease

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Stress-dependent cardiac remodeling occurs in the absence of microRNA-21 in mice

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A Family of microRNAs Encoded by Myosin Genes Governs Myosin Expression and Muscle Performance

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MicroRNA-21 protects against the H2O2-induced injury on cardiac myocytes via its target gene PDCD4

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Cardiac anti-remodelling effect of aerobic training is associated with a reduction in the calcineurin/NFAT signalling pathway in heart failure mice

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AT1 receptor participates in the cardiac hypertrophy induced by resistance training in rats

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MicroRNAs miR-186 and miR-150 Down-regulate Expression of the Pro-apoptotic Purinergic P2X7Receptor by Activation of Instability Sites at the 3′-Untranslated Region of the Gene That Decrease Steady-state Levels of the Transcript

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Deletion of GSK-3β in mice leads to hypertrophic cardiomyopathy secondary to cardiomyoblast hyperproliferation

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

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