Key result
Hyperosmolar stress drives proinflammatory renal macrophage activation and end-organ damage in salt-sensitive hypertension.
Why the study?
The role of inflammatory macrophages in the kidney and their contribution to salt-sensitive hypertension and renal damage is not fully understood, with a need to explore targeted modulation of specific signaling molecules to prevent end-organ damage.
Findings remain preclinical and should not guide therapy; leaves open hyperosmolarity's role in human salt-sensitive hypertension.
, 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.
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Fehrenbach et al. (2020) conducted a review in Salt-sensitive hypertension. Inflammatory macrophages was evaluated. In animal models of salt-sensitive hypertension, a hyperosmotic environment drives renal macrophages toward a proinflammatory phenotype, contributing to end-organ renal damage.
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