This work aims to validate the hypothesis that 1) TGFβ1 stimulation in combination with a hypoxia-mimicking compound (IOX2) exacerbates the HSC fibrotic phenotype through fibrotic markers (Collagen, TIMP-1, Fibronectin), and collagen crosslinks (pyridinoline/collagen), and 2) in vitro mimicking HIF-1α signaling improves the translational relevance of a primary human HSC model for liver fibrosis. This evidence concerns the gene TGFB1 and Hepatic fibrosis.