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Redox Biology of Right-Sided Heart Failure
Right-sided heart failure is the major cause of death among patients who suffer from various forms of pulmonary hypertension and congenital heart disease. The right ventricle (RV) and left ventricle (LV) originate from different progenitor cells and function against very different blood pressures. H...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2018
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6115847/ https://www.ncbi.nlm.nih.gov/pubmed/30096794 http://dx.doi.org/10.3390/antiox7080106 |
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author | Shults, Nataliia V. Melnyk, Oleksiy Suzuki, Dante I. Suzuki, Yuichiro J. |
author_facet | Shults, Nataliia V. Melnyk, Oleksiy Suzuki, Dante I. Suzuki, Yuichiro J. |
author_sort | Shults, Nataliia V. |
collection | PubMed |
description | Right-sided heart failure is the major cause of death among patients who suffer from various forms of pulmonary hypertension and congenital heart disease. The right ventricle (RV) and left ventricle (LV) originate from different progenitor cells and function against very different blood pressures. However, differences between the RV and LV formed after birth have not been well defined. Work from our laboratory and others has accumulated evidence that redox signaling, oxidative stress and antioxidant regulation are important components that define the RV/LV differences. The present article summarizes the progress in understanding the roles of redox biology in the RV chamber-specificity. Understanding the mechanisms of RV/LV differences should help develop selective therapeutic strategies to help patients who are susceptible to and suffering from right-sided heart failure. Modulations of redox biology may provide effective therapeutic avenues for these conditions. |
format | Online Article Text |
id | pubmed-6115847 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-61158472018-08-31 Redox Biology of Right-Sided Heart Failure Shults, Nataliia V. Melnyk, Oleksiy Suzuki, Dante I. Suzuki, Yuichiro J. Antioxidants (Basel) Review Right-sided heart failure is the major cause of death among patients who suffer from various forms of pulmonary hypertension and congenital heart disease. The right ventricle (RV) and left ventricle (LV) originate from different progenitor cells and function against very different blood pressures. However, differences between the RV and LV formed after birth have not been well defined. Work from our laboratory and others has accumulated evidence that redox signaling, oxidative stress and antioxidant regulation are important components that define the RV/LV differences. The present article summarizes the progress in understanding the roles of redox biology in the RV chamber-specificity. Understanding the mechanisms of RV/LV differences should help develop selective therapeutic strategies to help patients who are susceptible to and suffering from right-sided heart failure. Modulations of redox biology may provide effective therapeutic avenues for these conditions. MDPI 2018-08-08 /pmc/articles/PMC6115847/ /pubmed/30096794 http://dx.doi.org/10.3390/antiox7080106 Text en © 2018 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Review Shults, Nataliia V. Melnyk, Oleksiy Suzuki, Dante I. Suzuki, Yuichiro J. Redox Biology of Right-Sided Heart Failure |
title | Redox Biology of Right-Sided Heart Failure |
title_full | Redox Biology of Right-Sided Heart Failure |
title_fullStr | Redox Biology of Right-Sided Heart Failure |
title_full_unstemmed | Redox Biology of Right-Sided Heart Failure |
title_short | Redox Biology of Right-Sided Heart Failure |
title_sort | redox biology of right-sided heart failure |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6115847/ https://www.ncbi.nlm.nih.gov/pubmed/30096794 http://dx.doi.org/10.3390/antiox7080106 |
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