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Schematic depiction of the antifibrosis function of CKI by rebalancing TGFβ/Smad7 signaling to inhibit HSCs activation. CKI targeted Smad7 and facilitated the interaction between Smad7 and TGF‐β receptor, which inhibited the phosphorylation of Smad2 and Smad3 to suppress the downstream TGFβ signaling. As a result, CKI prevented HSCs activation, subsequently interdicted extracellular matrix production to inhibit chronic liver fibrosis and finally postponed hepatocarcinogenesis
