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 language | English (US) |
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Pages (from-to) | F544-F548 |
Journal | American Journal of Physiology - Renal Physiology |
Volume | 318 |
Issue number | 3 |
DOIs | |
State | Published - Mar 2022 |
Keywords
- inflammation
- kidney
- macrophage
- salt
ASJC Scopus subject areas
- Physiology
- Urology