Centrosomal protein 72 deficiency exacerbates liver fibrosis induced by Schistosoma japonicum infection.

backgroundHepatic fibrosis induced by Schistosoma japonicum (S. japonicum) infection is a major global public health concern. Centrosomal protein 72 (CEP72), a key regulator involved in maintaining cellular architecture and integrity, is significantly upregulated during the progression of hepatic fibrosis; however, its specific biological function in this pathological process remains largely elusive. This study was designed to elucidate the novel biological role of CEP72 in liver fibrosis, with a particular focus on the pathogenesis of S. japonicum-induced hepatic fibrosis.

methodsPublicly available transcriptomic datasets of human hepatic fibrosis were analyzed, and the key findings were validated in two murine models of liver fibrosis (S. japonicum infection and carbon tetrachloride (CCl

resultsCEP72 expression was significantly elevated in both human fibrotic liver samples and murine models of hepatic fibrosis. Notably, CEP72 deficiency markedly exacerbated liver fibrosis, as evidenced by significantly increased granuloma size and enhanced collagen deposition in both S. japonicum-infected and CCl

conclusionsCollectively, our findings demonstrate that CEP72 functions as a key negative regulator of inflammation-driven hepatic fibrosis. CEP72 deficiency accelerates the progression of liver fibrosis through the EGR1-TNF-α signaling pathway. This study identifies a previously unrecognized protective role of CEP72 in hepatic fibrosis and highlights its potential as a novel therapeutic target for the treatment of S. japonicum-induced and other types of inflammation-associated liver fibrosis.