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-specifi...

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Bibliographic Details
Published in:Journal of molecular and cellular cardiology 2016-05, Vol.94, p.107-121
Main Authors: Chistiakov, Dimitry A, Orekhov, Alexander N, Bobryshev, Yuri V
Format: Article
Language:English
Subjects:
Animals
Calcium Signaling
Cardiovascular
Cell Differentiation
Embryonic Stem Cells - cytology
Embryonic Stem Cells - metabolism
Gene Expression Regulation
Heart
Heart - embryology
Heart - physiology
Heart Diseases - diagnosis
Heart Diseases - genetics
Heart Diseases - physiopathology
Humans
MicroRNAs - genetics
miR-1
miR-133a
miR-208a/b
miR-499
Myocardial infarction
Myocardial Infarction - diagnosis
Myocardial Infarction - genetics
Myocardial Infarction - physiopathology
Myocardium - cytology
Myocardium - metabolism
Myocytes, Cardiac - cytology
Myocytes, Cardiac - metabolism
Organ Specificity
Oxidative Stress
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Summary: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.
ISSN:0022-2828
1095-8584
DOI:10.1016/j.yjmcc.2016.03.015