The role of chemokines in hypertension and consequent target organ damage.


Journal Article (Review)

Immune cells infiltrate the kidney, vasculature, and central nervous system during hypertension, consequently amplifying tissue damage and/or blood pressure elevation. Mononuclear cell motility depends partly on chemokines, which are small cytokines that guide cells through an increasing concentration gradient via ligation of their receptors. Tissue expression of several chemokines is elevated in clinical and experimental hypertension. Likewise, immune cells have enhanced chemokine receptor expression during hypertension, driving immune cell infiltration and inappropriate inflammation in cardiovascular control centers. T lymphocytes and monocytes/macrophages are pivotal mediators of hypertensive inflammation, and these cells migrate in response to several chemokines. As powerful drivers of diapedesis, the chemokines CCL2 and CCL5 have long been implicated in hypertension, but experimental data highlight divergent, context-specific effects of these chemokines on blood pressure and tissue injury. Several other chemokines, particularly those of the CXC family, contribute to blood pressure elevation and target organ damage. Given the significant interplay and chemotactic redundancy among chemokines during disease, future work must not only describe the actions of individual chemokines in hypertension, but also characterize how manipulating a single chemokine modulates the expression and/or function of other chemokines and their cognate receptors. This information will facilitate the design of precise chemotactic immunotherapies to limit cardiovascular and renal morbidity in hypertensive patients.

Full Text

Duke Authors

Cited Authors

  • Rudemiller, NP; Crowley, SD

Published Date

  • May 2017

Published In

Volume / Issue

  • 119 /

Start / End Page

  • 404 - 411

PubMed ID

  • 28279813

Pubmed Central ID

  • 28279813

Electronic International Standard Serial Number (EISSN)

  • 1096-1186

Digital Object Identifier (DOI)

  • 10.1016/j.phrs.2017.02.026


  • eng

Conference Location

  • Netherlands