Abstract
MicroRNAs (miRNAs) have emerged as potent modulators of mammalian gene expression, thereby broadening the spectrum of molecular mechanisms orchestrating human physiological and pathological cellular functions. Growing evidence suggests that these small non-coding RNA molecules are pivotal regulators of cardiovascular development and disease. Importantly, multiple miRNAs have been specifically implicated in the onset and progression of heart failure, thus providing a new platform for battling this multi-faceted disease. This review introduces the basic concepts of miRNA biology, describes representative examples of miRNAs associated with multiple aspects of HF pathogenesis, and explores the prognostic, diagnostic and therapeutic potential of miRNAs in the cardiology clinic.
Highlights
Heart failure (HF) is a complex clinical syndrome that may arise as a consequence of a spectrum of structural and functional cardiac abnormalities, as well as rhythm and conduction disorders.[1]
Studies conducted in the left ventricles of a rat model of hypertrophy induced by banding of the ascending aorta, detected four upregulated miRNAs, 14 days post operation, when the hypertrophy was already established.[93]
Some of the altered miRNAs were further associated with hypertrophy, CMC proliferation, cardiac electrophysiology, calcium signaling, fibrosis, and the TGF-b pathway, based on their predicted interaction with the dysregulated transcripts and the Gene Ontology annotations of the latter.[75]. These findings suggest that miRNAs play a critical role in the cardiac pathophysiology of the DBL mouse model during end-stage hypertrophic cardiomyopathy (HCM)
Summary
Heart failure (HF) is a complex clinical syndrome that may arise as a consequence of a spectrum of structural and functional cardiac abnormalities, as well as rhythm and conduction disorders.[1]. Survival after diagnosis has improved over time, studies show that roughly 50% of diagnosed HF patients will die within 5 years.[3,4,5] Systolic dysfunction is considered the most common underlying pathology of HF, and it may occur as a result of ischemic cardiac disease (coronary artery disease, CAD, myocardial infarction, MI) and/or hypertension, idiopathic dilated cardiomyopathy (DCM), hypertrophic cardiomyopathy (HCM) and valve lesions.[1] Extensive molecular studies have revealed multiple genetic and epigenetic factors implicated in the aforementioned primary pathologies.[6,7,8,9,10] MiRNAs are emerging as important regulators of gene expression that act to modulate numerous biological properties, under normal and pathological conditions As such, their role in the cardiovascular system and HF in specific is being thoroughly investigated, with direct implications in our understanding of the cardiac molecular physiology/pathophysiology and future molecular therapeutic targeting of HF
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
