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The mechanisms by which heme oxygenase (HO) improves glucose metabolism in essential hypertension are not completely understood. Because dysfunctional insulin signaling is associated with elevated inflammation and high cholesterol and triglycerides, we investigated the effects of HO on the proinflammatory macrophage M1 phenotype and the anti-inflammatory macrophage M2 phenotype in spontaneously hypertensive rats (SHRs). SHRs are a model of human essential hypertension with features of metabolic syndrome, including impaired glucose metabolism.

american journal of hypertension

The Heme Oxygenase System Selectively Suppresses the Proinflammatory Macrophage M1 Phenotype and Potentiates Insulin Signaling in Spontaneously Hypertensive Rats