title: Cardiac-specific miRNA in cardiogenesis, heart function, and cardiac pathology (with focus on myocardial infarction).
abstract: Cardiac miRNAs (miR-1, miR133a, miR-208a/b, and miR-499) are abundantly expressed in the myocardium. They play a central role in cardiogenesis, heart function and pathology. While miR-1 and miR-133a predominantly control early stages of cardiogenesis supporting commitment of cardiac-specific muscle lineage from embryonic stem cells and mesodermal precursors, miR-208 and miR-499 are involved in the late cardiogenic stages mediating differentiation of cardioblasts to cardiomyocytes and fast/slow muscle fiber specification. In the heart, miR-1/133a control cardiac conductance and automaticity by regulating all phases of the cardiac action potential. miR-208/499 located in introns of the heavy chain myosin genes regulate expression of sarcomeric contractile proteins. In cardiac pathology including myocardial infarction (MI), expression of cardiac miRNAs is markedly altered that leads to deleterious effects associated with heart wounding, arrhythmia, increased apoptosis, fibrosis, hypertrophy, and tissue remodeling. In acute MI, circulating levels of cardiac miRNAs are significantly elevated making them to be a promising diagnostic marker for early diagnosis of acute MI. Great cardiospecific capacity of these miRNAs is very helpful for enhancing regenerative properties and survival of stem cell and cardiac progenitor transplants and for reprogramming of mature non-cardiac cells to cardiomyocytes.
authors.affiliation: Department of Molecular Genetic Diagnostics and Cell Biology, Division of Laboratory Medicine, Institute of Pediatrics, Research Center for Children's Health, 119991 Moscow, Russia.
authors.forename: Dimitry A
authors.initials: DA
authors.lastname: Chistiakov
authors.affiliation: Institute of General Pathology and Pathophysiology, Russian Academy of Sciences, Moscow 125315, Russia; Department of Biophysics, Biological Faculty, Moscow State University, Moscow 119991, Russia; Institute for Atherosclerosis Research, Skolkovo Innovative Center, Moscow 121609, Russia.
authors.forename: Alexander N
authors.initials: AN
authors.lastname: Orekhov
authors.affiliation: Institute of General Pathology and Pathophysiology, Russian Academy of Sciences, Moscow 125315, Russia; Faculty of Medicine, School of Medical Sciences, University of New South Wales, Sydney, NSW 2052, Australia; School of Medicine, University of Western Sydney, Campbelltown, NSW 2560, Australia. Electronic address: y.bobryshev@unsw.edu.au.
authors.forename: Yuri V
authors.initials: YV
authors.lastname: Bobryshev
mesh_terms: D000818:Animals; D020013:Calcium Signaling; D002454:Cell Differentiation; D053595:Embryonic Stem Cells / Q000166:cytology / Q000378:metabolism; D005786:Gene Expression Regulation; D006321:Heart / Q000196:embryology* / Q000502:physiology*; D006331:Heart Diseases / Q000175:diagnosis / Q000235:genetics* / Q000503:physiopathology*; D006801:Humans; D035683:MicroRNAs / Q000235:genetics; D009203:Myocardial Infarction / Q000175:diagnosis / Q000235:genetics / Q000503:physiopathology; D009206:Myocardium / Q000166:cytology / Q000378:metabolism*; D032383:Myocytes, Cardiac / Q000166:cytology / Q000378:metabolism; D009928:Organ Specificity; D018384:Oxidative Stress
chemical_list: D035683:MicroRNAs
keywords: Heart; Myocardial infarction; miR-1; miR-133a; miR-208a/b; miR-499