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      Cellular and molecular basis of RV hypertrophy in congenital heart disease

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          Abstract

          RV hypertrophy (RVH) is one of the triggers of RV failure in congenital heart disease (CHD). Therefore, improving our understanding of the cellular and molecular basis of this pathology will help in developing strategic therapeutic interventions to enhance patient benefit in the future. This review describes the potential mechanisms that underlie the transition from RVH to RV failure. In particular, it addresses structural and functional remodelling that encompass contractile dysfunction, metabolic changes, shifts in gene expression and extracellular matrix remodelling. Both ischaemic stress and reactive oxygen species production are implicated in triggering these changes and will be discussed. Finally, RV remodelling in response to various CHDs as well as the potential role of biomarkers will be addressed.

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          The right ventricle under pressure: cellular and molecular mechanisms of right-heart failure in pulmonary hypertension.

          Harm J. Bogaard, Kohtaro Abe, Anton Vonk Noordegraaf … (2009)
          Pulmonary arterial hypertension (PAH) is a deadly disease in which vasoconstriction and vascular remodeling both lead to a progressive increase in pulmonary vascular resistance. The response of the right ventricle (RV) to the increased afterload is an important determinant of patient outcome. Little is known about the cellular and molecular mechanisms that underlie the transition from compensated hypertrophy to dilatation and failure that occurs during the course of the disease. Moreover, little is known about the direct effects of current PAH treatments on the heart. Although the increase in afterload is the first trigger for RV adaptation in PAH, neurohormonal signaling, oxidative stress, inflammation, ischemia, and cell death may contribute to the development of RV dilatation and failure. Here we review cellular signaling cascades and gene expression patterns in the heart that follow pressure overload. Most data are derived from research on the left ventricle, but where possible specific information on the RV response to pressure overload is provided. This overview identifies the gaps in our understanding of RV failure and attempts to fill them, when possible. Together with the online supplement, it provides a starting point for new research and aims to encourage the pulmonary hypertension research community to direct some of their attention to the RV, in parallel to their focus on the pulmonary vasculature.
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            Right versus left ventricular failure: differences, similarities, and interactions.

            Andrew N. Redington, M Friedberg (2014)
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              Changes in gene expression in the intact human heart. Downregulation of alpha-myosin heavy chain in hypertrophied, failing ventricular myocardium.

              Paul Gilbert, W Minobe, Mazen M Rizeq … (1997)
              Using quantitative RT-PCR in RNA from right ventricular (RV) endomyocardial biopsies from intact nonfailing hearts, and subjects with moderate RV failure from primary pulmonary hypertension (PPH) or idiopathic dilated cardiomyopathy (IDC), we measured expression of genes involved in regulation of contractility or hypertrophy. Gene expression was also assessed in LV (left ventricular) and RV free wall and RV endomyocardium of hearts from end-stage IDC subjects undergoing heart transplantation or from nonfailing donors. In intact failing hearts, downregulation of beta1-receptor mRNA and protein, upregulation of atrial natriuretic peptide mRNA expression, and increased myocyte diameter indicated similar degrees of failure and hypertrophy in the IDC and PPH phenotypes. The only molecular phenotypic difference between PPH and IDC RVs was upregulation of beta2-receptor gene expression in PPH but not IDC. The major new findings were that (a) both nonfailing intact and explanted human ventricular myocardium expressed substantial amounts of alpha-myosin heavy chain mRNA (alpha-MHC, 23-34% of total), and (b) in heart failure alpha-MHC was downregulated (by 67-84%) and beta-MHC gene expression was upregulated. We conclude that at the mRNA level nonfailing human heart expresses substantial alpha-MHC. In myocardial failure this alteration in gene expression of MHC isoforms, if translated into protein expression, would decrease myosin ATPase enzyme velocity and slow speed of contraction.
              Article 0 comments Cited 85 times – based on 0 reviews     Review now
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                Author and article information

                Journal
                Journal ID (nlm-ta): Heart
                Journal ID (iso-abbrev): Heart
                Journal ID (hwp): heartjnl
                Journal ID (publisher-id): heart
                Title: Heart
                Publisher: BMJ Publishing Group (BMA House, Tavistock Square, London, WC1H 9JR )
                ISSN (Print): 1355-6037
                ISSN (Electronic): 1468-201X
                Publication date (Print): 1 January 2016
                Publication date (Electronic): 29 October 2015
                Volume: 102
                Issue: 1
                Pages: 12-17
                Affiliations
                [1 ]School of Clinical Sciences, Bristol Royal Infirmary , Bristol, UK
                [2 ]Department of Congenital Heart Disease, Bristol Royal Hospital for Children, Bristol, UK
                Author notes
                [Correspondence to ] Professor RM Tulloh, Department of Congenital Heart Disease, Bristol Royal Hospital for Children, King David Building, Upper Maudlin Street, Bristol BS2 8BJ, UK; robert.tulloh@ 123456bristol.ac.uk
                Article
                Publisher ID: heartjnl-2015-308348
                DOI: 10.1136/heartjnl-2015-308348
                PMC ID: 4717403
                PubMed ID: 26516182
                SO-VID: d18f7169-ff95-49d4-a90a-f38f882b9d73
                Copyright © Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://www.bmj.com/company/products-services/rights-and-licensing/
                License:

                This is an Open Access article distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/

                History
                Date received : 9 July 2015
                Date revision received : 1 September 2015
                Date accepted : 11 September 2015
                Categories
                Subject: Review
                Subject: 1506
                Subject: 2269
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                ScienceOpen disciplines: Cardiovascular Medicine
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                ScienceOpen disciplines: Cardiovascular Medicine

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