Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2023 Mar 1;32(2):111-117.
doi: 10.1097/MNH.0000000000000862. Epub 2022 Dec 7.

Targeting inflammation in hypertension

Andreas Deussen  1 , Irakli Kopaliani
Affiliations
Review

Targeting inflammation in hypertension

Andreas Deussen et al. Curr Opin Nephrol Hypertens. .

Abstract

Purpose of review: 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.

PubMed Disclaimer

Conflict of interest statement

There are no conflicts of interest.

Figures

Box 1
Box 1
no caption available
FIGURE 1
FIGURE 1
Schematic model of interleukin interaction in mediation of hypertensive renal inflammation and injury.
FIGURE 2
FIGURE 2
Cross-talk of APC and T-cells, as well as role of memory T-cells in mediation of endothelial dysfunction during hypertension. APC, antigen-presenting cell.
FIGURE 3
FIGURE 3
Model mechanisms of anti-inflammatory actions of DEL-1 in hypertension. DEL-1, developmental endothelial locus-1.
See this image and copyright information in PMC

References

    1. Kearney PM, Whelton M, Reynolds K, et al. . Global burden of hypertension: analysis of worldwide data. Lancet 2005; 365:217–223. - PubMed
    1. Murray CJL, Lopez AD. Measuring the global burden of disease. New En J Med 2013; 369:448–457. - PubMed
    1. Beghi E, Giussani G, Abd-Allah F, et al. . Global, regional, and national burden of epilepsy, 1990–2016: a systematic analysis for the Global Burden of Disease Study. Lancen Neurol 2019; 18:357–375. - PMC - PubMed
    1. WheltonPK, Carey RM, Aronow W, Setal, et al. . 2017 ACC/AHA/AAPA/ABC/ACPM/AGS/APhA/ASH/ASPC/NMA/PCNA guideline for the prevention, detection, evaluation, and management of high blood pressure in adults: a report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines. Hypertension 2018; 71:e13–e115. - PubMed
    1. Page IH. The mosaic theory 32 years later. Hypertension 1982; 4:177. - PubMed

MeSH terms

Substances