Fig. 1

miRNAs regulate the HSC activation and schistosomiasis liver fibrosis through modulating TGF-β/SMAD signaling pathway. The key event of schistosomiasis liver fibrosis is the HSC activation, where the TGF-β/SMAD signaling pathway plays a vital role in the process. After schistosome infection, soluble egg antigen (SEA) induces macrophages to secret TGF-β [119, 120], which is the classic fibrogenic cytokine that promotes the activation of HSC. TGF-β binds to the receptors leading to phosphorylation of Smad-2 and Smad-3, followed by aggregation with Smad-4 and subsequently drives the expression of Smad-7 which negatively regulates TGF-β/SMAD signaling by blocking the TGF-β type I receptor (TβRΙ). Upon HSC activation, synthesis of ECM proteins is enhanced, especially collagen I and II, therefore resulting in liver fibrosis. Dysregulation of miRNAs regulate the TGF-β/SMAD signaling pathway to influence the activation of HSC and therefore exert a pro-fibrosis (miR-21, miR-96 and miR-351) or anti-fibrosis (miR-203-3p, miR-454, let-7b and miR-29b-3p) role in schistosomiasis