Extended Data Fig. 9: Pharmacological inhibition of Yap signaling ameliorates kidney fibrosis and promotes mitochondrial OXPHOS. | Nature Metabolism

Extended Data Fig. 9: Pharmacological inhibition of Yap signaling ameliorates kidney fibrosis and promotes mitochondrial OXPHOS.

From: Early-activated extracellular matrix proteins shape the metabolic and spatial dynamics of the kidney fibrotic microenvironment

Extended Data Fig. 9: Pharmacological inhibition of Yap signaling ameliorates kidney fibrosis and promotes mitochondrial OXPHOS.The alternative text for this image may have been generated using AI.

(a) qPCR analysis showing Tead1, Tead2, Tead3, and Tead4 mRNA levels in vehicle (Veh.) and VT103-treated kidneys after IRI (n = 5). (b) Quantitative data for the protein expression of COL1A1, FN, and α-SMA in vehicle and VT103-treated kidneys after IRI (n = 5). (c) Quantitative data for MTS and immunohistochemical staining (α-SMA, COL1A1, and CD45) in vehicle and VT103-treated mice kidneys after IRI (Sham, n = 3; IRI, n = 5). (d) Quantitative data for the protein expression of SDHB and NDUFB8 in vehicle and VT103-treated mice kidneys after IRI (n = 5). Data are presented as mean ± s.e.m. Differences between groups were analyzed using two-sided unpaired t tests or one-way ANOVA followed by the Student-Newman-Keuls test.

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