Unveiling MiRNA-124 as a biomarker in hypertrophic cardiomyopathy: An innovative approach using machine learning and intelligent data analysis.

Background: Hypertrophic cardiomyopathy (HCM) is a widespread hereditary cardiac pathology characterized by thickened heart walls and rearrangement of cardiomyocytes. Despite extensive research, the mechanisms underlying HCM development remain poorly understood, impeding the development of effective therapeutic and diagnostic strategies. Recent studies have suggested a polygenic nature of HCM development alongside monogenic forms.

Regulation of SMAD Signaling Pathway by miRNAs Associated with Myocardial Fibrosis: In silico Analysis of Target Gene Networks.

Hypertrophic cardiomyopathy (HCM) is a hereditary heart disease caused by mutations in the sarcomere genes, which is accompanied by myocardial fibrosis leading to progressive heart failure and arrhythmias. Recent studies suggest that the HCM development involves dysregulation of gene expression. Among the molecules involved in this process are microRNAs (miRNAs), which are short non-coding RNAs.

MiRNA-Regulated Pathways for Hypertrophic Cardiomyopathy: Network-Based Approach to Insight into Pathogenesis.

Hypertrophic cardiomyopathy (HCM) is the most common hereditary heart disease. The wide spread of high-throughput sequencing casts doubt on its monogenic nature, suggesting the presence of mechanisms of HCM development independent from mutations in sarcomeric genes. From this point of view, HCM may arise from the interactions of several HCM-associated genes, and from disturbance of regulation of their expression.

Analysis of MicroRNA Profile Alterations in Extracellular Vesicles From Mesenchymal Stromal Cells Overexpressing Stem Cell Factor.

Mesenchymal stem/stromal cells (MSCs) represent a promising tool to treat cardiovascular diseases. One mode of action through which MSCs exert their protective effects is secretion of extracellular vesicles (EVs). Recently, we demonstrated that rat adipose-derived MSC-overexpressing stem cell factor (SCF) can induce endogenous regenerative processes and improve cardiac function.

From miRNA Target Gene Network to miRNA Function: miR-375 Might Regulate Apoptosis and Actin Dynamics in the Heart Muscle via Rho-GTPases-Dependent Pathways.

MicroRNAs (miRNAs) are short, single-stranded, non-coding ribonucleic acid (RNA) molecules, which are involved in the regulation of main biological processes, such as apoptosis or cell proliferation and differentiation, through sequence-specific interaction with target mRNAs. In this study, we propose a workflow for predicting miRNAs function by analyzing the structure of the network of their target genes. This workflow was applied to study the functional role of miR-375 in the heart muscle (myocardium), since this miRNA was previously shown to be associated with heart diseases, and data on its function in the myocardium are mostly unclear.

Collapsing the list of myocardial infarction-related differentially expressed genes into a diagnostic signature.

Background: Myocardial infarction (MI) is one of the most severe manifestations of coronary artery disease (CAD) and the leading cause of death from non-infectious diseases worldwide. It is known that the central component of CAD pathogenesis is a chronic vascular inflammation. However, the mechanisms underlying the changes that occur in T, B and NK lymphocytes, monocytes and other immune cells during CAD and MI are still poorly understood.

MiRNAs from Imprinted Locus at 14q32 are Associated with Multiple Sclerosis: Gender-Specific Expression and Regulation of Receptor Tyrosine Kinases Signaling.

Relapsing-remitting multiple sclerosis (RRMS) is the most prevalent course of multiple sclerosis. It is an autoimmune inflammatory disease of the central nervous system. To investigate the gender-specific involvement of microRNAs (miRNAs) in RRMS pathogenesis, we compared miRNA profiles in peripheral blood mononuclear cells separately in men and women (eight RRMS patients versus four healthy controls of each gender) using high-throughput sequencing.

NGS-identified circulating miR-375 as a potential regulating component of myocardial infarction associated network.

Acute myocardial infarction (MI), the most severe type of coronary heart disease, is a leading cause of disability and mortality worldwide. In order to investigate the involvement of miRNAs in the pathologic processes related to MI, we performed the analysis of circulating miRNAs - stable short noncoding RNA molecules - in the peripheral blood plasma of MI patients compared to healthy controls (all persons were men and lived in European Russia) using next generation sequencing. We observed 20 miRNAs, which levels in plasma more than two-fold differed in MI patients (p < 0.

Impact of 9p21.3 region and atherosclerosis-related genes' variants on long-term recurrent hard cardiac events after a myocardial infarction.

Atherosclerotic coronary artery disease (CAD) and myocardial infarction (MI) as its most severe clinical complication remain the leading causes of mortality in the majority of countries. Despite the progress in the treatment of MI, quite often the patients, after the first-time MI, develop subsequently a variety of adverse cardiovascular events. In this retrospective study we evaluated the contribution of allelic variations in 9p21.

Immune-related miRNA expression patterns in peripheral blood mononuclear cells differ in multiple sclerosis relapse and remission.

MiRNAs were shown to participate in development of autoimmune inflammatory process in multiple sclerosis (MS). To investigate miRNAs involvement in relapse-remission MS course, we analyzed expression of immune-related miRNAs in PBMC of treatment-naïve relapsing and remitting MS patients and healthy controls. The upregulation of miR-126-3p, miR-146b-5p, miR-155, miR-196a-5p, miR-21-5p, miR-223-3p, miR-326 and miR-379-5p in remission compared to relapse was observed; when apply gender stratification, miR-223-3p and miR-379-5p were upregulated only in men.

Genetic risk factors for myocardial infarction more clearly manifest for early age of first onset.

Epidemiological genetics established that heritability in determining the risk of myocardial infarction (MI) is substantially greater when MI occurs early in life. However, the genetic architecture of early-onset and late-onset MI was not compared. We analyzed genotype frequencies of SNPs in/near 20 genes whose protein products are involved in the pathogenesis of atherosclerosis in two groups of Russian patients with MI: the first group included patients with age of first MI onset <60 years (N = 230) and the second group with onset ≥60 years (N = 174).

Variants of the Coagulation and Inflammation Genes Are Replicably Associated with Myocardial Infarction and Epistatically Interact in Russians.

Background: In spite of progress in cardiovascular genetics, data on genetic background of myocardial infarction are still limited and contradictory. This applies as well to the genes involved in inflammation and coagulation processes, which play a crucial role in the disease etiopathogenesis.

Methods And Results: In this study we found genetic variants of TGFB1, FGB and CRP genes associated with myocardial infarction in discovery and replication groups of Russian descent from the Moscow region and the Republic of Bashkortostan (325/185 and 220/197 samples, correspondingly).