HIF1A and Hepatic fibrosis: We further demonstrated that the PlGF, which was induced by hypoxia during liver fibrosis dependent on HIF‐1α, was involved in HSC activation and proliferation through modulation of the PI3K/Akt signalling pathway (Fig. 8), while the addition of PI3K inhibitor to PlGF‐treated HSCs abrogated the proliferative and activated effects of PlGF.