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Fig. 10 | Journal of Biomedical Science

Fig. 10

From: The down-regulation of XBP1, an unfolded protein response effector, promotes acute kidney injury to chronic kidney disease transition

Fig. 10

The mechanism for the involvement of the XBP1-Trap1 axis in post-AKI fibrosis. Our results show that AKI induces UPR activation as demonstrated by increased expression of p-PERK, cATF6, and p-IRE1. However, the expression of XBP1 is downregulated and is coincident with decreased expression of Trap1 and elevated expression of α-SMA and fibrosis progression. XBP1 directly regulates Trap1 expression. Restoration of Trap1 expression can alleviate the loss of XBP1 causes prolonged G2/M cell cycle arrest, relieves profibrotic factors expression, and ameliorates renal fibrosis progression

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