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ROCK Inhibition as Potential Target for Treatment of Pulmonary Hypertension

Pulmonary hypertension (PH) is a cardiovascular disease caused by extensive vascular remodeling in the lungs, which ultimately leads to death in consequence of right ventricle (RV) failure. While current drugs for PH therapy address the sustained vasoconstriction, no agent effectively targets vascul...

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Autores principales: Montagnoli, Tadeu L., da Silva, Jaqueline S., Sudo, Susumu Z., Santos, Aimeé D., Gomide, Gabriel F., de Sá, Mauro P. L., Zapata-Sudo, Gisele
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8303917/
https://www.ncbi.nlm.nih.gov/pubmed/34209333
http://dx.doi.org/10.3390/cells10071648
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author Montagnoli, Tadeu L.
da Silva, Jaqueline S.
Sudo, Susumu Z.
Santos, Aimeé D.
Gomide, Gabriel F.
de Sá, Mauro P. L.
Zapata-Sudo, Gisele
author_facet Montagnoli, Tadeu L.
da Silva, Jaqueline S.
Sudo, Susumu Z.
Santos, Aimeé D.
Gomide, Gabriel F.
de Sá, Mauro P. L.
Zapata-Sudo, Gisele
author_sort Montagnoli, Tadeu L.
collection PubMed
description Pulmonary hypertension (PH) is a cardiovascular disease caused by extensive vascular remodeling in the lungs, which ultimately leads to death in consequence of right ventricle (RV) failure. While current drugs for PH therapy address the sustained vasoconstriction, no agent effectively targets vascular cell proliferation and tissue inflammation. Rho-associated protein kinases (ROCKs) emerged in the last few decades as promising targets for PH therapy, since ROCK inhibitors demonstrated significant anti-remodeling and anti-inflammatory effects. In this review, current aspects of ROCK inhibition therapy are discussed in relation to the treatment of PH and RV dysfunction, from cell biology to preclinical and clinical studies.
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spelling pubmed-83039172021-07-25 ROCK Inhibition as Potential Target for Treatment of Pulmonary Hypertension Montagnoli, Tadeu L. da Silva, Jaqueline S. Sudo, Susumu Z. Santos, Aimeé D. Gomide, Gabriel F. de Sá, Mauro P. L. Zapata-Sudo, Gisele Cells Review Pulmonary hypertension (PH) is a cardiovascular disease caused by extensive vascular remodeling in the lungs, which ultimately leads to death in consequence of right ventricle (RV) failure. While current drugs for PH therapy address the sustained vasoconstriction, no agent effectively targets vascular cell proliferation and tissue inflammation. Rho-associated protein kinases (ROCKs) emerged in the last few decades as promising targets for PH therapy, since ROCK inhibitors demonstrated significant anti-remodeling and anti-inflammatory effects. In this review, current aspects of ROCK inhibition therapy are discussed in relation to the treatment of PH and RV dysfunction, from cell biology to preclinical and clinical studies. MDPI 2021-06-30 /pmc/articles/PMC8303917/ /pubmed/34209333 http://dx.doi.org/10.3390/cells10071648 Text en © 2021 by the authors. https://creativecommons.org/licenses/by/4.0/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 (https://creativecommons.org/licenses/by/4.0/).
spellingShingle Review
Montagnoli, Tadeu L.
da Silva, Jaqueline S.
Sudo, Susumu Z.
Santos, Aimeé D.
Gomide, Gabriel F.
de Sá, Mauro P. L.
Zapata-Sudo, Gisele
ROCK Inhibition as Potential Target for Treatment of Pulmonary Hypertension
title ROCK Inhibition as Potential Target for Treatment of Pulmonary Hypertension
title_full ROCK Inhibition as Potential Target for Treatment of Pulmonary Hypertension
title_fullStr ROCK Inhibition as Potential Target for Treatment of Pulmonary Hypertension
title_full_unstemmed ROCK Inhibition as Potential Target for Treatment of Pulmonary Hypertension
title_short ROCK Inhibition as Potential Target for Treatment of Pulmonary Hypertension
title_sort rock inhibition as potential target for treatment of pulmonary hypertension
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8303917/
https://www.ncbi.nlm.nih.gov/pubmed/34209333
http://dx.doi.org/10.3390/cells10071648
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