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. 2022 May 18;19(1):256–277. doi: 10.1080/15548627.2022.2072054

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This work was authored as part of the Contributor’s official duties as an Employee of the United States Government and is therefore a work of the United States Government. In accordance with 17 USC. 105, no copyright protection is available for such works under US Law.

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Figure 1. — Autophagy is persistently activated in renal tubular cells during maladaptive kidney repair after ischemic AKI in mice. C57BL/6 mice underwent sham operation (n = 4) or 30-min unilateral renal ischemia followed by reperfusion for up to 4 weeks (n = 8). Left kidneys were harvested at the indicated time points. (A) Masson’s trichrome staining. Scale bar: 50 µm. (B) LC3B immunoblot. (C) Autophagy reporter mice (CAG-RFP-GFP-LC3) underwent sham operation (n = 7) or 30-min unilateral renal ischemia followed by reperfusion for up to 4 weeks (n = 4 to 6 for each time point). Left kidneys were harvested for confocal microscopy of autophagosomes and autolysosomes in renal tubules. Scale bar: 15 µm. (D) Quantification of the numbers of autophagosomes and autolysosomes per proximal tubule. (E) Quantification of autophagic flux rate. Data in (D and E) are presented as mean ± SD. For statistics, two-way ANOVA with multiple comparisons was used for (D). One-way ANOVA with multiple comparisons was used for (E).