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Pulmonary hypertension: Linking inflammation and pulmonary arterial stiffening

Pulmonary hypertension (PH) is a progressive disease that arises from multiple etiologies and ultimately leads to right heart failure as the predominant cause of morbidity and mortality. In patients, distinct inflammatory responses are a prominent feature in different types of PH, and various immuno...

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Autores principales: Liu, Shao-Fei, Nambiar Veetil, Netra, Li, Qiuhua, Kucherenko, Mariya M., Knosalla, Christoph, Kuebler, Wolfgang M.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9579293/
https://www.ncbi.nlm.nih.gov/pubmed/36275740
http://dx.doi.org/10.3389/fimmu.2022.959209
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author Liu, Shao-Fei
Nambiar Veetil, Netra
Li, Qiuhua
Kucherenko, Mariya M.
Knosalla, Christoph
Kuebler, Wolfgang M.
author_facet Liu, Shao-Fei
Nambiar Veetil, Netra
Li, Qiuhua
Kucherenko, Mariya M.
Knosalla, Christoph
Kuebler, Wolfgang M.
author_sort Liu, Shao-Fei
collection PubMed
description Pulmonary hypertension (PH) is a progressive disease that arises from multiple etiologies and ultimately leads to right heart failure as the predominant cause of morbidity and mortality. In patients, distinct inflammatory responses are a prominent feature in different types of PH, and various immunomodulatory interventions have been shown to modulate disease development and progression in animal models. Specifically, PH-associated inflammation comprises infiltration of both innate and adaptive immune cells into the vascular wall of the pulmonary vasculature—specifically in pulmonary vascular lesions—as well as increased levels of cytokines and chemokines in circulating blood and in the perivascular tissue of pulmonary arteries (PAs). Previous studies suggest that altered hemodynamic forces cause lung endothelial dysfunction and, in turn, adherence of immune cells and release of inflammatory mediators, while the resulting perivascular inflammation, in turn, promotes vascular remodeling and the progression of PH. As such, a vicious cycle of endothelial activation, inflammation, and vascular remodeling may develop and drive the disease process. PA stiffening constitutes an emerging research area in PH, with relevance in PH diagnostics, prognostics, and as a therapeutic target. With respect to its prognostic value, PA stiffness rivals the well-established measurement of pulmonary vascular resistance as a predictor of disease outcome. Vascular remodeling of the arterial extracellular matrix (ECM) as well as vascular calcification, smooth muscle cell stiffening, vascular wall thickening, and tissue fibrosis contribute to PA stiffening. While associations between inflammation and vascular stiffening are well-established in systemic vascular diseases such as atherosclerosis or the vascular manifestations of systemic sclerosis, a similar connection between inflammatory processes and PA stiffening has so far not been addressed in the context of PH. In this review, we discuss potential links between inflammation and PA stiffening with a specific focus on vascular calcification and ECM remodeling in PH.
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spelling pubmed-95792932022-10-20 Pulmonary hypertension: Linking inflammation and pulmonary arterial stiffening Liu, Shao-Fei Nambiar Veetil, Netra Li, Qiuhua Kucherenko, Mariya M. Knosalla, Christoph Kuebler, Wolfgang M. Front Immunol Immunology Pulmonary hypertension (PH) is a progressive disease that arises from multiple etiologies and ultimately leads to right heart failure as the predominant cause of morbidity and mortality. In patients, distinct inflammatory responses are a prominent feature in different types of PH, and various immunomodulatory interventions have been shown to modulate disease development and progression in animal models. Specifically, PH-associated inflammation comprises infiltration of both innate and adaptive immune cells into the vascular wall of the pulmonary vasculature—specifically in pulmonary vascular lesions—as well as increased levels of cytokines and chemokines in circulating blood and in the perivascular tissue of pulmonary arteries (PAs). Previous studies suggest that altered hemodynamic forces cause lung endothelial dysfunction and, in turn, adherence of immune cells and release of inflammatory mediators, while the resulting perivascular inflammation, in turn, promotes vascular remodeling and the progression of PH. As such, a vicious cycle of endothelial activation, inflammation, and vascular remodeling may develop and drive the disease process. PA stiffening constitutes an emerging research area in PH, with relevance in PH diagnostics, prognostics, and as a therapeutic target. With respect to its prognostic value, PA stiffness rivals the well-established measurement of pulmonary vascular resistance as a predictor of disease outcome. Vascular remodeling of the arterial extracellular matrix (ECM) as well as vascular calcification, smooth muscle cell stiffening, vascular wall thickening, and tissue fibrosis contribute to PA stiffening. While associations between inflammation and vascular stiffening are well-established in systemic vascular diseases such as atherosclerosis or the vascular manifestations of systemic sclerosis, a similar connection between inflammatory processes and PA stiffening has so far not been addressed in the context of PH. In this review, we discuss potential links between inflammation and PA stiffening with a specific focus on vascular calcification and ECM remodeling in PH. Frontiers Media S.A. 2022-10-05 /pmc/articles/PMC9579293/ /pubmed/36275740 http://dx.doi.org/10.3389/fimmu.2022.959209 Text en Copyright © 2022 Liu, Nambiar Veetil, Li, Kucherenko, Knosalla and Kuebler https://creativecommons.org/licenses/by/4.0/This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Immunology
Liu, Shao-Fei
Nambiar Veetil, Netra
Li, Qiuhua
Kucherenko, Mariya M.
Knosalla, Christoph
Kuebler, Wolfgang M.
Pulmonary hypertension: Linking inflammation and pulmonary arterial stiffening
title Pulmonary hypertension: Linking inflammation and pulmonary arterial stiffening
title_full Pulmonary hypertension: Linking inflammation and pulmonary arterial stiffening
title_fullStr Pulmonary hypertension: Linking inflammation and pulmonary arterial stiffening
title_full_unstemmed Pulmonary hypertension: Linking inflammation and pulmonary arterial stiffening
title_short Pulmonary hypertension: Linking inflammation and pulmonary arterial stiffening
title_sort pulmonary hypertension: linking inflammation and pulmonary arterial stiffening
topic Immunology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9579293/
https://www.ncbi.nlm.nih.gov/pubmed/36275740
http://dx.doi.org/10.3389/fimmu.2022.959209
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