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      New Insights and Current Approaches in Cardiac Hypertrophy Cell Culture, Tissue Engineering Models, and Novel Pathways Involving Non-Coding RNA

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          Abstract

          Cardiac hypertrophy is an ongoing clinical challenge, as risk factors such as obesity, smoking and increasing age become more widespread, which lead to an increasing prevalence of developing hypertrophy. Pathological hypertrophy is a maladaptive response to stress conditions, such as pressure overload, and involve a number of changes in cellular mechanisms, gene expression and pathway regulations. Although several important pathways involved in the remodeling and hypertrophy process have been identified, further research is needed to achieve a better understanding and explore new and better treatment options. More recently discovered pathways showed the involvement of several non-coding RNAs, including micro RNAs (miRNAs), long non-coding RNAs (lncRNAs), and circular RNAs (circRNAs), which either promote or inhibit the remodeling process and pose a possible target for novel therapy approaches. In vitro modeling serves as a vital tool for this further pathway analysis and treatment testing and has vastly improved over the recent years, providing a less costly and labor-intensive alternative to in vivo animal models.

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          Most cited references49

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          Cardiac Fibrosis: The Fibroblast Awakens.

          Myocardial fibrosis is a significant global health problem associated with nearly all forms of heart disease. Cardiac fibroblasts comprise an essential cell type in the heart that is responsible for the homeostasis of the extracellular matrix; however, upon injury, these cells transform to a myofibroblast phenotype and contribute to cardiac fibrosis. This remodeling involves pathological changes that include chamber dilation, cardiomyocyte hypertrophy and apoptosis, and ultimately leads to the progression to heart failure. Despite the critical importance of fibrosis in cardiovascular disease, our limited understanding of the cardiac fibroblast impedes the development of potential therapies that effectively target this cell type and its pathological contribution to disease progression. This review summarizes current knowledge regarding the origins and roles of fibroblasts, mediators and signaling pathways known to influence fibroblast function after myocardial injury, as well as novel therapeutic strategies under investigation to attenuate cardiac fibrosis.
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            Mechanisms of physiological and pathological cardiac hypertrophy

            Cardiomyocytes exit the cell cycle and become terminally differentiated soon after birth. Therefore, in the adult heart, instead of an increase in cardiomyocyte number, individual cardiomyocytes increase in size, and the heart develops hypertrophy to reduce ventricular wall stress and maintain function and efficiency in response to an increased workload. There are two types of hypertrophy: physiological and pathological. Hypertrophy initially develops as an adaptive response to physiological and pathological stimuli, but pathological hypertrophy generally progresses to heart failure. Each form of hypertrophy is regulated by distinct cellular signalling pathways. In the past decade, a growing number of studies have suggested that previously unrecognized mechanisms, including cellular metabolism, proliferation, non-coding RNAs, immune responses, translational regulation, and epigenetic modifications, positively or negatively regulate cardiac hypertrophy. In this Review, we summarize the underlying molecular mechanisms of physiological and pathological hypertrophy, with a particular emphasis on the role of metabolic remodelling in both forms of cardiac hypertrophy, and we discuss how the current knowledge on cardiac hypertrophy can be applied to develop novel therapeutic strategies to prevent or reverse pathological hypertrophy.
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              The mechanics of miRNA-mediated gene silencing: a look under the hood of miRISC.

              Since their discovery almost two decades ago, microRNAs (miRNAs) have been shown to function by post-transcriptionally regulating protein accumulation. Understanding how miRNAs silence targeted mRNAs has been the focus of intensive research. Multiple models have been proposed, with few mechanistic details having been worked out. However, the past few years have witnessed a quantum leap forward in our understanding of the molecular mechanics of miRNA-mediated gene silencing. In this review we describe recent discoveries, with an emphasis on how miRISC post-transcriptionally controls gene expression by inhibiting translation and/or initiating mRNA decay, and how trans-acting factors control miRNA action.
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                Author and article information

                Contributors
                Journal
                Front Pharmacol
                Front Pharmacol
                Front. Pharmacol.
                Frontiers in Pharmacology
                Frontiers Media S.A.
                1663-9812
                21 August 2020
                2020
                : 11
                : 1314
                Affiliations
                [1]Department of Cardiology, Medical University of Vienna , Vienna, Austria
                Author notes

                Edited by: Hai-Gang Zhang, Army Medical University, China

                Reviewed by: Yong Zhang, Harbin Medical University, China; Ning Zhang, Affiliated Hospital of Qingdao University, China

                *Correspondence: Mariann Gyöngyösi, mariann.gyongyosi@ 123456meduniwien.ac.at

                This article was submitted to Cardiovascular and Smooth Muscle Pharmacology, a section of the journal Frontiers in Pharmacology

                †These authors have contributed equally to this work

                Article
                10.3389/fphar.2020.01314
                7472597
                dde1da2e-2eb8-4d9d-bc1e-0826ba707411
                Copyright © 2020 Kastner, Zlabinger, Spannbauer, Traxler, Mester-Tonczar, Hašimbegović and Gyöngyösi

                This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

                History
                : 04 June 2020
                : 07 August 2020
                Page count
                Figures: 0, Tables: 1, Equations: 0, References: 60, Pages: 7, Words: 3147
                Categories
                Pharmacology
                Mini Review

                Pharmacology & Pharmaceutical medicine
                cardiac hypertrophy,disease modeling,hypertrophy induction,non-coding rna,tissue engineering

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