TLR4 and metabolic dysfunction-associated steatohepatitis: HSCs engulfed NLRP3 particles increase IL-1β secretion and α-smooth muscle actin (α-SMA) expression, thereby inducing hepatic fibrosis (62). Moreover, Dong et al. found that NLRP3 activation in HSCs of mice exacerbated the progression of NASH to hepatic fibrosis through the TLR4-NF-κB signaling pathway (63).