Immune and inflammatory mechanisms in hypertension

Tomasz Guzik, Ryszard Nosalski, Pasquale Maffia, Grant R. Drummond

Research output: Contribution to journalArticlepeer-review

Abstract / Description of output

Hypertension is a global health problem, with >1.3 billion individuals with high blood pressure worldwide. In this Review, we present a novel 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 (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 (TH17) cells, and γδ T cells and interferon-γ (IFNγ) and tumour necrosis factor (TNF) 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.
Original languageEnglish
JournalNature Reviews Cardiology
Publication statusPublished - 3 Jan 2024


Dive into the research topics of 'Immune and inflammatory mechanisms in hypertension'. Together they form a unique fingerprint.

Cite this