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. 2023 Sep 26;24(19):14530. doi: 10.3390/ijms241914530

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© 2023 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).

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KLF15 expression is reduced in AKI mice, and KLF15 deficiency promotes renal injury in mice. (A,B) Serum CRE and BUN levels in each group. (C) Periodic acid-Schiff (PAS) staining showed a significant acute tubular injury in the FA kidney. (D) Protein and mRNA expression of KLF15 in kidney samples of FA mice. (E,F) Serum BUN and CRE levels in each group. (G) Representative images of PAS staining. (H) Protein expression of KIM-1 in kidney samples in each group. (I) KIM-1 and NGAL mRNA expression in kidney samples in each group. KLF15, Krüppel-like factor 15; CRE, creatinine; BUN, blood urea nitrogen; CON, control; FA, folic acid; KIM-1, kidney injury molecule 1; NGAL, neutrophil gelatinase-associated lipocalin. Data are shown as the mean ± SD (n = 5). Original magnification, ×400 for all. Scale bar = 50 μm. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.