Is microRNA(miRNA) 30 involved in post-ischemic cardiac remodeling?
['The myocardium of the failing heart undergoes a number of structural alterations, most notably hypertrophy of cardiac myocytes and an increase in extracellular matrix proteins, often seen as primary fibrosi', 'Connective tissue growth factor (CTGF) is a key molecule in the process of fibrosis and therefore seems an attractive therapeutic target', 'CTGF is importantly regulated by 2 major cardiac microRNAs (miRNAs), miR-133 and miR-30.', 'the expression of both miRNAs was inversely related to the amount of CTGF in 2 rodent models of heart disease and in human pathological left ventricular hypertrophy. Second, in cultured cardiomyocytes and fibroblasts, knockdown of these miRNAs increased CTGF levels. Third, overexpression of miR-133 or miR-30c decreased CTGF levels, which was accompanied by decreased production of collagens.', 'miR-30 importantly limit the production of CTGF', 'miR-30 directly downregulate CTGF, a key profibrotic protein, and thereby establish an important role for these miRNAs in the control of structural changes in the extracellular matrix of the myocardium.']
['Myocardial remodeling after an ischemic insult involves extracellular matrix proteins with increased fibrosis\nInitial experimental data indicate that miRNA 30 decreases CTGF a key molecule in the process of fibrosis, by directly downregulating the production of CTGF']
['yes']