SMAD2 and Hepatic fibrosis: In our study, mouse models of CCl4-induced liver fibrosis were injected with AAV–shLRRC1 vector via the tail vein to inhibit LRRC1 expression, and we found that knockdown of LRRC1 in vivo effectively mitigated CCl4-induced liver fibrosis, as evidenced by the reduction of collagen accumulation and the expressions of fibrogenic genes and p-Smad2/3, which aligns with our results in vitro.