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BioMed Research International
Volume 2018, Article ID 1981568, 10 pages
Review Article

Current Knowledge and Recent Advances of Right Ventricular Molecular Biology and Metabolism from Congenital Heart Disease to Chronic Pulmonary Hypertension

1Research and Innovation Unit, RHU BioArt Lung 2020, Marie Lannelongue Hospital, Paris-Sud University, Le Plessis-Robinson, France
2Cardiac Surgery, Marie Lannelongue Hospital, Paris-Sud University, Le Plessis-Robinson, France
3Division of Cardiovascular Medicine, Stanford Cardiovascular Institute, Stanford University School of Medicine, Stanford, CA, USA
4Thoracic and Vascular Surgery and Heart and Lung Transplantation, Marie Lannelongue Hospital, Paris-Sud University, Le Plessis-Robinson, France

Correspondence should be addressed to Julien Guihaire; moc.liamg@eriahiugneiluj

Received 1 September 2017; Accepted 20 December 2017; Published 17 January 2018

Academic Editor: Utako Yokoyama

Copyright © 2018 Samantha Guimaron et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Studies about pulmonary hypertension and congenital heart diseases have introduced the concept of right ventricular remodeling leading these pathologies to a similar outcome: right ventricular failure. However right ventricular remodeling is also a physiological process that enables the normal fetal right ventricle to adapt at birth and gain its adult phenotype. The healthy mature right ventricle is exposed to low pulmonary vascular resistances and is compliant. However, in the setting of chronic pressure overload, as in pulmonary hypertension, or volume overload, as in congenital heart diseases, the right ventricle reverts back to a fetal phenotype to sustain its function. Mechanisms include angiogenic changes and concomitant increased metabolic activity to maintain energy production. Eventually, the remodeled right ventricle cannot resist the increased afterload, leading to right ventricular failure. After comparing the fetal and adult healthy right ventricles, we sought to review the main metabolic and cellular changes occurring in the setting of PH and CHD. Their association with RV function and potential impact on clinical practice will also be discussed.