PPARγ, as a transcription factor, controls gene transcription and cell differentiation both in vitro and in vivo and plays a key role in inhibiting HSC activation and maintaining the morphological and biochemical reversal of activated HSC to quiescent cells [17–19]. Current evidences have shown that hypoxia is a common stimulus to the development of hepatic fibrosis and HSCs activation [20, 21]. In fact, hypoxia is capable of connecting a variety of signals. It not only affects the activation of HSCs but also acts on a variety of other cells, such as sinusoidal cells, hepatocytes, adipocytes, and liver-resident macrophages (Kuppfer cells) [1, 22–24]. Secondly, hypoxia-induced structural changes in hepatic fibrosis aggravate the hypoxic environment, thus, in turn, accelerating its pathologic progression of hepatic fibrosis.