Inflammatory macrophages in the kidney contribute to salt-sensitive hypertension

Daniel J. Fehrenbach, David L. Mattson

Research output: Contribution to journalReview article

Abstract

This review will highlight recent studies that have investigated the relationship between Na+, renal macrophage polarization, and renal damage. A hyperosmotic environment drives the macrophage toward a proinflammatory phenotype and away from an anti-inflammatory phenotype. Animal models of salt-sensitive hypertension demonstrate a characteristic infiltration of macrophages into the kidney that is greatly reduced when blood pressure is lowered. Because general immunosuppression or macrophage depletion leads to a host of adverse side effects, more recent studies have modulated the interaction of specific signaling molecules, including NOD-like receptor family pyrin domain-containing 3, chemokine (C-X-C motif) ligand 16, and VEGF, to prevent the end-organ renal damage that accumulates in salt-sensitive disease.

Original languageEnglish (US)
Pages (from-to)F544-F548
JournalAmerican journal of physiology. Renal physiology
Volume318
Issue number3
DOIs
StatePublished - Mar 1 2020

Keywords

  • inflammation
  • kidney
  • macrophage
  • salt

ASJC Scopus subject areas

  • Physiology
  • Urology

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