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MHA Winter Meeting 2018

(September 2017) The MHA Winter Meeting 2018 takes place on February 5th at the Carl Friedrich von Siemens Stiftung at Nymphenburg.

MiR-378 Controls Cardiac Hypertrophy by Combined Repression of MAP Kinase Pathway Factors

Transfection of miR-378 inhibits phenylephrine (PE)-induced hypertrophy of primary cardiomyocytes.

(April 2013) MicroRNAs (miRs) are small, noncoding RNAs that posttranscriptionally regulate gene expression. Thus, miRs have been shown to regulate many processes in health and disease, including cardiovascular disease. Using a method to screen libraries of mulitple synthetic miRs for the induction of cardiomyocyte hypertrophy, a hallmark of the myocardial stress response, a research team led by Stefan Engelhardt at the Institute of Pharmacology at TUM hat found the first evidence for an antihypertrophic activity of miR-378 in the myocardium. Subsequent analyses carried out by Jaya Ganesan, a PhD student at the Institute of Pharmacology and Toxicology now showed that miR-378 represses prohypertrophic signaling at four levels within the mitogen-activated protein kinase signaling pathway. MiR-378 was found to be downregulated both in animal models of myocardial disease and in human failing myocardium. Compensation for miR-378 downregulation in a cardiac disease model using viral gene transfer in vivo protected the heart against hypertrophy and dysfunction. Together, these data indicate effective interference of miR-378 with a key prohypertrophic signaling pathway. Targeted delivery of miR-378 to the heart may prove to be an effective therapeutic strategy in myocardial disease. For further reading see undefinedCirculation, published online April 26th, 2013.