During the initiation of fibrosis in vivo, CCl4 induced defenestration, a pro-fibrotic phenotype transition of LSECs, along with a time-dependent elevation of autophagy and depletion of Cav-1 in LSECs; while autophagy inhibitor 3MA inhibited these effects to maintain fenestrae and attenuated liver fibrosis. Here, CAV1 is linked to Hepatic fibrosis.