Figure 2.

The potential association between the ER stress signaling pathway and obesity. ER stress induced by a variety of factors activates the unfolded protein response (UPR). PERK, IRE1α, and ATF6α, located in the ER membrane, act as UPR messengers and maintain ER stability by coordinating protein production and gene expression. PERK reduces protein synthesis by modifying eIF2α and induces CHOP through ATF4 mRNA translation. IRE1α splices XBP1 mRNA to generate XBP1 and induces genes linked to ER function. XBP1 enhances ER membrane formation, protein folding, transport, and ERAD. ATF6α is processed in the Golgi by S1P and S2P to release p50ATF6α (cleaved ATF6), which is pivotal for genes involved in ER protein folding and processing. All of these processes are multifactorial and highly interlinked.