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Immune and inflammatory mechanisms in hypertension.
Guzik, Tomasz J; Nosalski, Ryszard; Maffia, Pasquale; Drummond, Grant R.
Afiliación
  • Guzik TJ; Centre for Cardiovascular Sciences, University of Edinburgh, Edinburgh, UK. tguzik@ed.ac.uk.
  • Nosalski R; Department of Medicine and Omicron Medical Genomics Laboratory, Jagiellonian University, Collegium Medicum, Kraków, Poland. tguzik@ed.ac.uk.
  • Maffia P; Africa-Europe Cluster of Research Excellence (CoRE) in Non-Communicable Diseases & Multimorbidity, African Research Universities Alliance ARUA & The Guild, Glasgow, UK. tguzik@ed.ac.uk.
  • Drummond GR; Centre for Cardiovascular Sciences, University of Edinburgh, Edinburgh, UK.
Nat Rev Cardiol ; 21(6): 396-416, 2024 06.
Article en En | MEDLINE | ID: mdl-38172242
ABSTRACT
Hypertension is a global health problem, with >1.3 billion individuals with high blood pressure worldwide. In this Review, we present an inflammatory paradigm for hypertension, emphasizing the crucial roles of immune cells, cytokines and chemokines in disease initiation and progression. T cells, monocytes, macrophages, dendritic cells, B cells and natural killer cells are all implicated in hypertension. Neoantigens, the NLRP3 inflammasome and increased sympathetic outflow, as well as cytokines (including IL-6, IL-7, IL-15, IL-18 and IL-21) and a high-salt environment, can contribute to immune activation in hypertension. The activated immune cells migrate to target organs such as arteries (especially the perivascular fat and adventitia), kidneys, the heart and the brain, where they release effector cytokines that elevate blood pressure and cause vascular remodelling, renal damage, cardiac hypertrophy, cognitive impairment and dementia. IL-17 secreted by CD4+ T helper 17 cells and γδ T cells, and interferon-γ and tumour necrosis factor secreted by immunosenescent CD8+ T cells, exert crucial effector roles in hypertension, whereas IL-10 and regulatory T cells are protective. Effector mediators impair nitric oxide bioavailability, leading to endothelial dysfunction and increased vascular contractility. Inflammatory effector mediators also alter renal sodium and water balance and promote renal fibrosis. These mechanisms link hypertension with obesity, autoimmunity, periodontitis and COVID-19. A comprehensive understanding of the immune and inflammatory mechanisms of hypertension is crucial for safely and effectively translating the findings to clinical practice.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Hipertensión / Inflamación Límite: Animals / Humans Idioma: En Revista: Nat Rev Cardiol Asunto de la revista: CARDIOLOGIA Año: 2024 Tipo del documento: Article País de afiliación: Reino Unido Pais de publicación: Reino Unido
Texto completo
Añadir a Mi BVS
Imprimir
XML
PubMed Links
Buscar en Google

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Hipertensión / Inflamación Límite: Animals / Humans Idioma: En Revista: Nat Rev Cardiol Asunto de la revista: CARDIOLOGIA Año: 2024 Tipo del documento: Article País de afiliación: Reino Unido Pais de publicación: Reino Unido