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The adventitia, vascular inflammation, and the intersection of hypertension and vascular disease

David G Harrison1

  • 1Division of Genetic Medicine and Clinical Pharmacology, Department of Medicine, Vanderbilt University Medical Center, Nashville, TN, 37232, USA.

Atherosclerosis
|August 7, 2026
PubMed

Insights

Hypertension drives vascular inflammation and stiffening through immune cell activation in the artery wall. Targeting these adventitial inflammation pathways offers a novel strategy for treating hypertension-associated cardiovascular disease.

Area of Science:

  • Cardiovascular Research
  • Immunology
  • Vascular Biology

Background:

  • Hypertension is a major risk factor for cardiovascular disease, linked to atherosclerosis via mechanical stress and inflammation.
  • The adventitia and perivascular adipose tissue are key sites for immune cell accumulation and cytokine release in hypertension.
  • Adventitial inflammation contributes to vascular stiffening and end-organ damage.

Purpose of the Study:

  • To review the cellular and molecular mechanisms connecting adventitial inflammation to vascular stiffening and end-organ damage in hypertension.
  • To explore the role of immune cells and cytokines in hypertension-induced vascular pathology.
  • To identify potential therapeutic targets within these inflammatory pathways.

Main Methods:

  • Review of existing literature on hypertension, cardiovascular disease, and inflammation.
  • Analysis of cellular and molecular mechanisms involving immune cells, chemokines, and cytokines.
  • Examination of pathways like p38 MAP kinase and oxidative stress in vascular disease.
  • Investigation of isolevuglandin (IsoLG)-protein adducts as neoantigens.

Main Results:

  • Hypertension promotes effector memory T cell accumulation in the adventitia, driven by chemokines like RANTES/CCL5.
  • Immune cell cytokines (IL-17A, IFN-γ) induce endothelial dysfunction, superoxide production, and collagen deposition via p38 MAP kinase.
  • Vascular oxidative stress generates IsoLG-protein adducts, activating immune cells and driving aortic stiffening.
  • Stiffened arteries impair cardiovascular function and promote further immune cell activation, leading to end-organ damage.

Conclusions:

  • Adventitial and perivascular inflammation are active drivers, not just consequences, of hypertension-related vascular disease.
  • Immune mechanisms create feed-forward loops that exacerbate vascular damage and end-organ injury.
  • Targeting adventitial inflammatory pathways presents a promising therapeutic strategy for hypertension-associated vascular complications.

Keywords:
AdventitiaAortic stiffnessCollagenIsolevuglandinsPerivascular adipose tissueT lymphocytes

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