Right versus left ventricular remodeling in heart failure due to chronic volume overload

Abstract Mechanisms of right ventricular (RV) dysfunction in heart failure (HF) are poorly understood. RV response to volume overload (VO), a common contributing factor to HF, is rarely studied. The goal was to identify interventricular differences in response to chronic VO. Rats underwent aorto-cav...

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Autores principales:	Tereza Havlenova, Petra Skaroupkova, Matus Miklovic, Matej Behounek, Martin Chmel, Dagmar Jarkovska, Jitka Sviglerova, Milan Stengl, Michal Kolar, Jiri Novotny, Jan Benes, Ludek Cervenka, Jiri Petrak, Vojtech Melenovsky
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2021
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/f251e8fd9382404c85c5d930444a3cba
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spelling	oai:doaj.org-article:f251e8fd9382404c85c5d930444a3cba2021-12-02T15:09:07ZRight versus left ventricular remodeling in heart failure due to chronic volume overload10.1038/s41598-021-96618-82045-2322https://doaj.org/article/f251e8fd9382404c85c5d930444a3cba2021-08-01T00:00:00Zhttps://doi.org/10.1038/s41598-021-96618-8https://doaj.org/toc/2045-2322Abstract Mechanisms of right ventricular (RV) dysfunction in heart failure (HF) are poorly understood. RV response to volume overload (VO), a common contributing factor to HF, is rarely studied. The goal was to identify interventricular differences in response to chronic VO. Rats underwent aorto-caval fistula (ACF)/sham operation to induce VO. After 24 weeks, RV and left ventricular (LV) functions, gene expression and proteomics were studied. ACF led to biventricular dilatation, systolic dysfunction and hypertrophy affecting relatively more RV. Increased RV afterload contributed to larger RV stroke work increment compared to LV. Both ACF ventricles displayed upregulation of genes of myocardial stress and metabolism. Most proteins reacted to VO in a similar direction in both ventricles, yet the expression changes were more pronounced in RV (pslope: < 0.001). The most upregulated were extracellular matrix (POSTN, NRAP, TGM2, CKAP4), cell adhesion (NCAM, NRAP, XIRP2) and cytoskeletal proteins (FHL1, CSRP3) and enzymes of carbohydrate (PKM) or norepinephrine (MAOA) metabolism. Downregulated were MYH6 and FAO enzymes. Therefore, when exposed to identical VO, both ventricles display similar upregulation of stress and metabolic markers. Relatively larger response of ACF RV compared to the LV may be caused by concomitant pulmonary hypertension. No evidence supports RV chamber-specific regulation of protein expression in response to VO.Tereza HavlenovaPetra SkaroupkovaMatus MiklovicMatej BehounekMartin ChmelDagmar JarkovskaJitka SviglerovaMilan StenglMichal KolarJiri NovotnyJan BenesLudek CervenkaJiri PetrakVojtech MelenovskyNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 11, Iss 1, Pp 1-16 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Tereza Havlenova Petra Skaroupkova Matus Miklovic Matej Behounek Martin Chmel Dagmar Jarkovska Jitka Sviglerova Milan Stengl Michal Kolar Jiri Novotny Jan Benes Ludek Cervenka Jiri Petrak Vojtech Melenovsky Right versus left ventricular remodeling in heart failure due to chronic volume overload
description	Abstract Mechanisms of right ventricular (RV) dysfunction in heart failure (HF) are poorly understood. RV response to volume overload (VO), a common contributing factor to HF, is rarely studied. The goal was to identify interventricular differences in response to chronic VO. Rats underwent aorto-caval fistula (ACF)/sham operation to induce VO. After 24 weeks, RV and left ventricular (LV) functions, gene expression and proteomics were studied. ACF led to biventricular dilatation, systolic dysfunction and hypertrophy affecting relatively more RV. Increased RV afterload contributed to larger RV stroke work increment compared to LV. Both ACF ventricles displayed upregulation of genes of myocardial stress and metabolism. Most proteins reacted to VO in a similar direction in both ventricles, yet the expression changes were more pronounced in RV (pslope: < 0.001). The most upregulated were extracellular matrix (POSTN, NRAP, TGM2, CKAP4), cell adhesion (NCAM, NRAP, XIRP2) and cytoskeletal proteins (FHL1, CSRP3) and enzymes of carbohydrate (PKM) or norepinephrine (MAOA) metabolism. Downregulated were MYH6 and FAO enzymes. Therefore, when exposed to identical VO, both ventricles display similar upregulation of stress and metabolic markers. Relatively larger response of ACF RV compared to the LV may be caused by concomitant pulmonary hypertension. No evidence supports RV chamber-specific regulation of protein expression in response to VO.
format	article
author	Tereza Havlenova Petra Skaroupkova Matus Miklovic Matej Behounek Martin Chmel Dagmar Jarkovska Jitka Sviglerova Milan Stengl Michal Kolar Jiri Novotny Jan Benes Ludek Cervenka Jiri Petrak Vojtech Melenovsky
author_facet	Tereza Havlenova Petra Skaroupkova Matus Miklovic Matej Behounek Martin Chmel Dagmar Jarkovska Jitka Sviglerova Milan Stengl Michal Kolar Jiri Novotny Jan Benes Ludek Cervenka Jiri Petrak Vojtech Melenovsky
author_sort	Tereza Havlenova
title	Right versus left ventricular remodeling in heart failure due to chronic volume overload
title_short	Right versus left ventricular remodeling in heart failure due to chronic volume overload
title_full	Right versus left ventricular remodeling in heart failure due to chronic volume overload
title_fullStr	Right versus left ventricular remodeling in heart failure due to chronic volume overload
title_full_unstemmed	Right versus left ventricular remodeling in heart failure due to chronic volume overload
title_sort	right versus left ventricular remodeling in heart failure due to chronic volume overload
publisher	Nature Portfolio
publishDate	2021
url	https://doaj.org/article/f251e8fd9382404c85c5d930444a3cba
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Right versus left ventricular remodeling in heart failure due to chronic volume overload

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