NR1H4 and metabolic dysfunction-associated steatotic liver disease: Building on quercetin’s framework, its metabolite isorhamnetin alleviated cholestasis and decelerated NAFLD progression by upregulating FXR-mediated BSEP to promote canalicular BA excretion, while OATP-1B3 suppression reduced sinusoidal reuptake, collectively shifting BA flux toward intestinal elimination to alleviate hepatic BA overload (La et al., 2024).