Figure 5: Disturbed cellular energy homeostasis in ADTKD-UMOD affected kidneys. | Scientific Reports

Figure 5: Disturbed cellular energy homeostasis in ADTKD-UMOD affected kidneys.

From: Mitochondrial Dysregulation Secondary to Endoplasmic Reticulum Stress in Autosomal Dominant Tubulointerstitial Kidney Disease – UMOD (ADTKD-UMOD)

Figure 5

(A) Z score heat maps showed differentially abundant proteins involved in OXPHOS, citrate cycle and glucose catabolic process. (B) The phosphorylation of AMPKα was increased in the outer medulla of UmodA227T and UmodC93F mutant mice compared to wild-type mice, indicating an impaired cellular energy homeostasis in ADTKD-UMOD. Protein abundance of AMPKα was similar between different genotypes. The phosphorylation of LKB1 was increased in the outer medulla of UmodA227T and UmodC93F mutant mice compared to wild-type mice, further supporting existence of energy depletion in ADTKD-UMOD. Protein abundance of LKB1 was similar between different genotypes. Also ATM abundance was similar irrespective of genotype. Signal intensities were corrected for GAPDH signal intensities of the same PVDF-membrane. Mean of protein abundance of wild-type mice was set on a value of 1 [mean (wild-type) = 1]. Data are shown as means ± SD. One-way ANOVA with Newman-Keuls’s post hoc test: p vs. wild-type, *p < 0.05; **p < 0.01; ***p < 0.001.

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