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The article presents a study on the importance of restoring MicroRNA (MiR)-133a to be able to regulate cardiac and skeletal muscle differentiation, reduced myocardial fibrosis and cardiomyocyte apoptosis in the U.S. The study intends to prevent the normal downregulation of miR-133a that is induced through the acute hypertrophic stimulus. The findings reveal of the unreliability of the mRNA signature to predict the miR targets.

The heart is among the most conserved organs of the body and is susceptible to defects more than any other organ. Heart malformations, in fact, occur in roughly 1% of newborns. Moreover, cardiovascular disease arising during adult life is among the main causes of morbidity and mortality in developed countries. It is not surprising, therefore, that much effort is being channeled into understanding the development, physiology, and pathology of the cardiovascular system. MicroRNAs, a newly discovered class of small ribonucleotide-based regulators of gene expression, are being implicated in an increasing number of biological processes, and the study of their role in cardiovascular biology is just beginning. Here, we briefly overview microRNAs in general and report on the recent findings regarding their importance for the heart and vasculature, in particular. The new insights that are being gained will permit not only a greater understanding of cardiovascular pathologies but also, hopefully, the development of novel therapeutic strategies. [ABSTRACT FROM AUTHOR]

The authors reflect on the ATP6V0A1 polymorphism which is considered as the common variant T3246C modifies gene expression through disparity binding to the microRNA (miR) 637. The authors states that miRs are considered essential components of eukaryotic gene expression, which are located in three untranslated regions of mRNAs. The authors suggest that the human adenosine triphosphatase (ATPase) mechanism must be considered its multigenetic nature of modulatory and essential hypertension.