Jens Heyn, Christian Hinske, Patrick Mohnle, Benjamin Luchting, Andres Beiras-Fernandez and Simone Kreth Pages 733 - 740 ( 8 )
In spite of enormous efforts, myocardial infarction is one of the most common causes of morbidity and mortality worldwide. The molecular mechanisms underlying the pathological myocardial alterations in affected patients are not fully elucidated. Recent studies have uncovered an important regulatory role for microRNAs (miRNAs), a family of small non-coding RNA molecules which - by translational repression or messenger RNA (mRNA) degradation - primarily act as negative regulators of gene expression. MiRNAs have been identified as regulatory key players during cellular differentiation, proliferation, and apoptosis. Recent work has unveiled an important impact of miRNAs on the pathophysiology of myocardial infarction and consecutive myocardial alterations, including arrhythmia, remodelling processes, cardiac fibrosis, and hypertrophia. Additionally, specific miRNAs have been identified to be either elevated or decreased in the blood plasma after myocardial infarction. Determination of miRNA expression levels therefore offers a potential prognostic and/or predictive value. Future therapeutic concepts aiming at attenuation of ischemia-induced harm and reduction of maladaptive changes may include strategies to influence altered miRNA expression patterns. In this review, we summarize current knowledge of the modulating role of miRNAs in pathological alterations occurring in myocardial infarction as well as currently available data concerning miRNAs as diagnostic markers and therapeutic targets.
miRNA, myocardial infarction, diagnostic marker, therapeutic target, cellular differentiation, proliferation, apoptosis, arrhythmia, VEGF, neoangiogenesis
Department of Anaesthesiology, University of Munich (LMU), Marchioninistrasse 15, D-81337 Munich, Germany.