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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| Format: | Article |
| Language: | English |
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Frontiers Media S.A.
2022-10-01
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| Series: | Frontiers in Immunology |
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| Online Access: | https://www.frontiersin.org/articles/10.3389/fimmu.2022.959209/full |
| _version_ | 1817969235264012288 |
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| author | Shao-Fei Liu Shao-Fei Liu Netra Nambiar Veetil Netra Nambiar Veetil Netra Nambiar Veetil Qiuhua Li Qiuhua Li Mariya M. Kucherenko Mariya M. Kucherenko Mariya M. Kucherenko Christoph Knosalla Christoph Knosalla Christoph Knosalla Wolfgang M. Kuebler Wolfgang M. Kuebler Wolfgang M. Kuebler Wolfgang M. Kuebler Wolfgang M. Kuebler |
| author_facet | Shao-Fei Liu Shao-Fei Liu Netra Nambiar Veetil Netra Nambiar Veetil Netra Nambiar Veetil Qiuhua Li Qiuhua Li Mariya M. Kucherenko Mariya M. Kucherenko Mariya M. Kucherenko Christoph Knosalla Christoph Knosalla Christoph Knosalla Wolfgang M. Kuebler Wolfgang M. Kuebler Wolfgang M. Kuebler Wolfgang M. Kuebler Wolfgang M. Kuebler |
| author_sort | Shao-Fei Liu |
| collection | DOAJ |
| 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. |
| first_indexed | 2024-04-13T20:18:46Z |
| format | Article |
| id | doaj.art-f5f145c36dd14044affe4a074d09d13f |
| institution | Directory Open Access Journal |
| issn | 1664-3224 |
| language | English |
| last_indexed | 2024-04-13T20:18:46Z |
| publishDate | 2022-10-01 |
| publisher | Frontiers Media S.A. |
| record_format | Article |
| series | Frontiers in Immunology |
| spelling | doaj.art-f5f145c36dd14044affe4a074d09d13f2022-12-22T02:31:38ZengFrontiers Media S.A.Frontiers in Immunology1664-32242022-10-011310.3389/fimmu.2022.959209959209Pulmonary hypertension: Linking inflammation and pulmonary arterial stiffeningShao-Fei Liu0Shao-Fei Liu1Netra Nambiar Veetil2Netra Nambiar Veetil3Netra Nambiar Veetil4Qiuhua Li5Qiuhua Li6Mariya M. Kucherenko7Mariya M. Kucherenko8Mariya M. Kucherenko9Christoph Knosalla10Christoph Knosalla11Christoph Knosalla12Wolfgang M. Kuebler13Wolfgang M. Kuebler14Wolfgang M. Kuebler15Wolfgang M. Kuebler16Wolfgang M. Kuebler17Institute of Physiology, Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, GermanyGerman Centre for Cardiovascular Research (DZHK), Berlin, GermanyInstitute of Physiology, Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, GermanyGerman Centre for Cardiovascular Research (DZHK), Berlin, GermanyDepartment of Cardiothoracic and Vascular Surgery, German Heart Center, Berlin, GermanyInstitute of Physiology, Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, GermanyGerman Centre for Cardiovascular Research (DZHK), Berlin, GermanyInstitute of Physiology, Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, GermanyGerman Centre for Cardiovascular Research (DZHK), Berlin, GermanyDepartment of Cardiothoracic and Vascular Surgery, German Heart Center, Berlin, GermanyGerman Centre for Cardiovascular Research (DZHK), Berlin, GermanyDepartment of Cardiothoracic and Vascular Surgery, German Heart Center, Berlin, GermanyCharité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, GermanyInstitute of Physiology, Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, GermanyGerman Centre for Cardiovascular Research (DZHK), Berlin, GermanyGerman Center for Lung Research (DZL), Gießen, GermanyThe Keenan Research Centre for Biomedical Science, St. Michael’s Hospital, Toronto, ON, CanadaDepartment of Surgery and Physiology, University of Toronto, Toronto, ON, CanadaPulmonary 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.https://www.frontiersin.org/articles/10.3389/fimmu.2022.959209/fullpulmonary hypertensioninflammationvascular stiffnessvascular calcificationECM remodeling |
| spellingShingle | Shao-Fei Liu Shao-Fei Liu Netra Nambiar Veetil Netra Nambiar Veetil Netra Nambiar Veetil Qiuhua Li Qiuhua Li Mariya M. Kucherenko Mariya M. Kucherenko Mariya M. Kucherenko Christoph Knosalla Christoph Knosalla Christoph Knosalla Wolfgang M. Kuebler Wolfgang M. Kuebler Wolfgang M. Kuebler Wolfgang M. Kuebler Wolfgang M. Kuebler Pulmonary hypertension: Linking inflammation and pulmonary arterial stiffening Frontiers in Immunology pulmonary hypertension inflammation vascular stiffness vascular calcification ECM remodeling |
| 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 | pulmonary hypertension inflammation vascular stiffness vascular calcification ECM remodeling |
| url | https://www.frontiersin.org/articles/10.3389/fimmu.2022.959209/full |
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