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Fig. 1 | Journal of Translational Medicine

Fig. 1

From: GCN5L1-mediated TFAM acetylation at K76 participates in mitochondrial biogenesis in acute kidney injury

Fig. 1

The expression of GCN5L1 is significantly upregulated in AKI and specific tubular GCN5L1 knockdown alleviates I/R-induced kidney damage. A, B Immunohistochemistry staining for GCN5L1 expression in kidney sections. C, D Immunohistochemistry staining for GCN5L1 expression in kidney sections of AKI mice model. E Representative photomicrographs of H/E, MASSON and PAS staining in kidney sections of AKI mice models. F, G Western blot analysis of GCN5L1 protein expression in hypoxia-reoxygenation induced TECs. H Positive correlation (Spearman r = 0.769, P = 0.003) between GCN5L1 IHC staining levels and serum creatinine in all subjects. I Positive correlation (Spearman r = 0.594, P = 0.042) between GCN5L1 IHC staining levels and BUN in all subjects. J Experimental design of GCN5L1 knockdown mice with acute kidney injury. K, L Western blot analysis for the expression of GCN5L1 in the kidneys from GCN5L1 knockdown mice with acute kidney injury. M, N Immunohistochemistry staining for GCN5L1 expression in kidney sections of mice. O Representative photomicrographs of H/E, MASSON and PAS staining in kidney sections of mice. P, Q Serum creatinine and BUN levels of GCN5L1 knockdown mice with acute kidney injury. *P < 0.05, **P < 0.01, and ***P < 0.001

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