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mtROS generation was assessed by measuring the fluorescence intensity of mito-SOX in a flow cytometry. Hypoxia significantly increased the fluorescence intensity of mito-SOX in ASCs (Figure 3A). Mito-CP (Figure 3B), a mitochondria specific ROS scavenger, was synthesized to investigate the involvement of mtROS generation in adipocyte differentiation. Compared to TPP treatment (as negative control), scavenging mtROS with mito-CP significantly reduced hypoxia-induced lipid accumulation in a dose-dependent manner [https://en.wikipedia.org/wiki/Ritipenem Ritipenem] (Figure 3C, P?[http://www.selleckchem.com/products/BI6727-Volasertib.html see more] signaling pathways activated by hypoxia (Figure 4A). Phosphorylation of ERK1/2, Akt, and mTOR was significantly increased by hypoxia (P?[http://www.selleckchem.com/products/cb-839.html check details] (Supplemental Fig. 2). The findings indicate that PI3K/Akt/mTOR pathway plays a pivotal regulatory role in adipocyte differentiation. The reported data should shed some light on important aspects of hypoxia-induced adipocyte differentiation of ASCs, as well as identify the cellular mechanisms of ROS-mediated adipocyte differentiation. Hypoxia (2% oxygen) induced adipocyte differentiation via ROS, but not RNS, generation. Furthermore, Nox4 inhibition or silencing did not inhibit adipocyte differentiation. However, hypoxia induced mtROS generation, and mito-CP (mtROS scavenger) treatment significantly reduced hypoxia-induced adipocyte differentiation. Hypoxia led to phosphorylation of Akt and mTOR, and inhibition of the PI3K/Akt/mTOR pathway inhibited adipocyte differentiation. Thus hypoxia induces adipocyte differentiation by mtROS generation, and the PI3K/Akt/mTOR pathway is involved in adipocyte differentiation of ASCs. Adipogenesis is triggered by signaling molecules that induce conversion of ASCs to preadipocytes that further differentiate into adipocytes (Cristancho and Lazar, 2011).