Soluble guanylate cyclase stimulator praliciguat attenuates inflammation, fibrosis, and end-organ damage in the Dahl model of cardiorenal failure

摘要

Nitric oxide (NO) binds and activates soluble guanylate cyclase (sGC) to increase the production of cGMP. Regulation of the NO-sGC-cGMP pathway is critical for normal cellular activity and physiological homeostasis (25). Increased oxida-tive stress and impaired NO signaling are associated with increased blood pressure (21), inflammation, and fibrosis in organs including the kidney (39), heart (30, 34), and liver (31). The inflammation and fibrosis associated with deficient NO signaling are linked to the pathogenesis of many renal, cardiovascular, and hepatic diseases.