MicroRNAs in Cardiac Hypertrophy
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MDPI AG
Abstract
Like other organs, the heart undergoes normal adaptive remodeling, such as cardiac hypertrophy, with age. This remodeling, however, is intensified under stress and pathological conditions. Cardiac remodeling could be beneficial for a short period of time, to maintain a normal cardiac output in times of need; however, chronic cardiac hypertrophy may lead to heart failure and death. MicroRNAs (miRNAs) are known to have a role in the regulation of cardiac hypertrophy. This paper reviews recent advances in the field of miRNAs and cardiac hypertrophy, highlighting the latest findings for targeted genes and involved signaling pathways. By targeting pro-hypertrophic genes and signaling pathways, some of these miRNAs alleviate cardiac hypertrophy, while others enhance it. Therefore, miRNAs represent very promising potential pharmacotherapeutic targets for the management and treatment of cardiac hypertrophy. © 2019 by the authors. Licensee MDPI, Basel, Switzerland.
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Cardiac hypertrophy, Cardiac remodeling, Cardiomyocytez, Micrornas, Therapeutic targets, Animals, Cardiomegaly, Heart failure, Humans, Signal transduction, Cyclin d2, Diacylglycerol, Microrna, Microrna 1, Microrna 10a, Microrna 124, Microrna 125b, Microrna 133, Microrna 139, Microrna 15, Microrna 150, Microrna 16, Microrna 19, Microrna 195, Microrna 200c, Microrna 206, Microrna 208a, Microrna 23, Microrna 24, Microrna 29, Microrna 297, Microrna 320, Microrna 499, Microrna 590, Mitogen activated protein kinase, Serum response factor, Small interfering rna, Stat3 protein, Suppressor of cytokine signaling 1, Transcription factor, Unclassified drug, Apoptosis, Autophagy, Cardiac muscle cell, Cell cycle progression, Cell division, Cell proliferation, Dna methylation, Dna recombination, Down regulation, Endoplasmic reticulum stress, Gene overexpression, Genetic transcription, Heart ventricle hypertrophy, Human, Mrna expression level, Muscle contractility, Nonhuman, Protein expression, Review, Transcription regulation, Upregulation, Animal, Metabolism, Pathology