PTGER4 and metabolic dysfunction-associated steatohepatitis: In the HBV-infected liver, endogenous PGE2 induced M1 polarization of macrophages and suppressed M2 polarization via EP4 receptors, leading to increased inflammation and aggravation of the nonalcoholic steatohepatitis (NASH) phenotype, while the EP4 antagonist, to some extent, improved the disturbance of lipid accumulation in the liver and balanced Kupffer cell polarization [169].