Abstract

The last decades showed a worrying increase in the evolution of cardiovascular diseases towards different stages of heart failure (HF), as a stigma of the western lifestyle. MicroRNAs (miRNAs), non-coding RNAs, which are approximately 22-nucleotide long, were shown to regulate gene expression at the post-transcriptional level and play a role in the pathogenesis and progression of HF. miRNAs research is of high interest nowadays, as these molecules display mechanisms of action that can influence the course of evolution of common chronic diseases, including HF. The potential of post-transcriptional regulation by miRNAs concerning the diagnosis, management, and therapy for HF represents a new promising approach in the accurate assessment of cardiovascular diseases. This review aims to assess the current knowledge of miRNAs in cardiovascular diseases, especially right-sided heart failure and hepatomegaly. Moreover, attention is focused on their role as potential molecular biomarkers and more promising aspects involving miRNAs as future therapeutic targets in the pathophysiology of HF.

Highlights

  • Cardiovascular diseases, heart failure (HF) included, result from numerous interactions from diverse genomic, genetic, environmental factors and lifestyle

  • From the hugeness of information related to miRNAs, this review aims to point out the most important discoveries related to their usefulness in heart failure, with greater emphasis on right heart failure accompanied by hepatomegaly

  • The study aimed to determine miRNAs that could point into the direction of important liver fibrosis in Univentricular heart disease (UHD) patients [85]. miR-29b-3p and miR-29c-3p proved to be best related to the Model for End-stage Liver Disease (MELD)-Albumin and Albumin-Bilirubin (ALBI) scores, being in higher concentrations in patients with MELD-Albumin scores over 11 and ALBI scores over -2.6, indicating fibrosis or cirrhosis of the liver [85]

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Summary

Introduction

Cardiovascular diseases, heart failure (HF) included, result from numerous interactions from diverse genomic, genetic, environmental factors and lifestyle. One of the leading causes of mortality and morbidity worldwide, is defined by the American Heart Association and American College of Cardiology as a complex clinical syndrome that can result from any structural or functional cardiac disorder that impairs the ability of the ventricle to fill with or eject blood”. HF most often occurs as the last stage of decompensation of many pre-existing disorders, such as chronic high blood pressure, coronary artery disease, myocardial infarction, myocarditis, mitral regurgitation by overload, drug abuse, or as a result of chemotherapy. Some other factors such as congenital heart defects, abnormal heart valves, diabetes, sleep apnea, and alcohol abuse can contribute [2]

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