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Significance Nonalcoholic steatohepatitis (NASH) is an increasingly common disease characterized by liver steatosis and inflammation—with fibrosis being an important indicator of disease progression and severity—and is associated with reduced endothelial function and NO–soluble guanylate cyclase (sGC) signaling. Signaling downstream of NO can be restored using praliciguat, an sGC stimulator. Within the liver, stellate cells and myofibroblasts express sGC (unlike hepatocytes) and thus can be stimulated by praliciguat. Increased sGC activity inhibits fibrotic transformation and inflammatory responses in stellate cells potentially through AMPK and SMAD7. The effects on isolated stellate cells translate to human microtissues and in vivo models where treatment with praliciguat reduces inflammation, fibrosis, and steatosis. These preclinical results support further investigation of praliciguat as a potential therapy for NASH/fibrosis.

sGC stimulator praliciguat suppresses stellate cell fibrotic transformation and inhibits fibrosis and inflammation in models of NASH