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Targeting inflammation in hypertension

Hypertension remains a global health and socioeconomic burden. Immune mechanisms are now recognized as integral part of the multifactorial etiology of hypertension and related organ damage. The present review addresses inflammatory pathways and immune targets in hypertension, which may be important...

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Detalles Bibliográficos
Autores principales: Deussen, Andreas, Kopaliani, Irakli
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Lippincott Williams & Wilkins 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9872860/
https://www.ncbi.nlm.nih.gov/pubmed/36476561
http://dx.doi.org/10.1097/MNH.0000000000000862
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author Deussen, Andreas
Kopaliani, Irakli
author_facet Deussen, Andreas
Kopaliani, Irakli
author_sort Deussen, Andreas
collection PubMed
description Hypertension remains a global health and socioeconomic burden. Immune mechanisms are now recognized as integral part of the multifactorial etiology of hypertension and related organ damage. The present review addresses inflammatory pathways and immune targets in hypertension, which may be important for an immunomodulatory treatment of hypertension aside from lowering arterial pressure. RECENT FINDINGS: Anti-inflammatory interventions targeting single interleukins or almost the entire immune system show different beneficial effects. While immunomodulation (targeting specific portion of immune system) shows beneficial outcomes in certain groups of hypertensives, this does not pertain to immunosuppression (targeting entire immune system). Immunomodulatory interventions improve outcomes of hypertension independent of arterial pressure. The studies reveal interleukins, such as interleukin (IL)-1β and IL-17 as targets of immunomodulation. Besides interleukins, targeting αvβ-3 integrin and matrix metalloproteinase-2 or using experimental cell-therapy demonstrate beneficial effects in hypertensive organ damage. The NLR family pyrin domain containing 3 (NLRP3) inflammasome/IL-1β/endothelial cell/T-cell axis seems to be an important mediator in sustained inflammation during hypertension. SUMMARY: Although immunomodulation may be advantageous as a causal therapy in hypertension, targeting immune networks rather than single interleukins appears of major importance. Further research is required to better identify these networks and their links to human hypertension.
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spelling pubmed-98728602023-01-27 Targeting inflammation in hypertension Deussen, Andreas Kopaliani, Irakli Curr Opin Nephrol Hypertens PATHOPHYSIOLOGY OF HYPERTENSION: Edited by Nancy J. Brown Hypertension remains a global health and socioeconomic burden. Immune mechanisms are now recognized as integral part of the multifactorial etiology of hypertension and related organ damage. The present review addresses inflammatory pathways and immune targets in hypertension, which may be important for an immunomodulatory treatment of hypertension aside from lowering arterial pressure. RECENT FINDINGS: Anti-inflammatory interventions targeting single interleukins or almost the entire immune system show different beneficial effects. While immunomodulation (targeting specific portion of immune system) shows beneficial outcomes in certain groups of hypertensives, this does not pertain to immunosuppression (targeting entire immune system). Immunomodulatory interventions improve outcomes of hypertension independent of arterial pressure. The studies reveal interleukins, such as interleukin (IL)-1β and IL-17 as targets of immunomodulation. Besides interleukins, targeting αvβ-3 integrin and matrix metalloproteinase-2 or using experimental cell-therapy demonstrate beneficial effects in hypertensive organ damage. The NLR family pyrin domain containing 3 (NLRP3) inflammasome/IL-1β/endothelial cell/T-cell axis seems to be an important mediator in sustained inflammation during hypertension. SUMMARY: Although immunomodulation may be advantageous as a causal therapy in hypertension, targeting immune networks rather than single interleukins appears of major importance. Further research is required to better identify these networks and their links to human hypertension. Lippincott Williams & Wilkins 2023-03 2022-12-07 /pmc/articles/PMC9872860/ /pubmed/36476561 http://dx.doi.org/10.1097/MNH.0000000000000862 Text en Copyright © 2022 The Author(s). Published by Wolters Kluwer Health, Inc. https://creativecommons.org/licenses/by-nc-nd/4.0/This is an open access article distributed under the terms of the Creative Commons Attribution-Non Commercial-No Derivatives License 4.0 (CCBY-NC-ND), where it is permissible to download and share the work provided it is properly cited. The work cannot be changed in any way or used commercially without permission from the journal. http://creativecommons.org/licenses/by-nc-nd/4.0 (https://creativecommons.org/licenses/by-nc-nd/4.0/)
spellingShingle PATHOPHYSIOLOGY OF HYPERTENSION: Edited by Nancy J. Brown
Deussen, Andreas
Kopaliani, Irakli
Targeting inflammation in hypertension
title Targeting inflammation in hypertension
title_full Targeting inflammation in hypertension
title_fullStr Targeting inflammation in hypertension
title_full_unstemmed Targeting inflammation in hypertension
title_short Targeting inflammation in hypertension
title_sort targeting inflammation in hypertension
topic PATHOPHYSIOLOGY OF HYPERTENSION: Edited by Nancy J. Brown
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9872860/
https://www.ncbi.nlm.nih.gov/pubmed/36476561
http://dx.doi.org/10.1097/MNH.0000000000000862
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