Fig. 2

Myeloid autophagy-related 5 (Atg5) deletion inhibited macrophage migration into the kidneys in early acute ischemic injury. Wild-type (WT) and MΦ atg5^−/− mice underwent 26 min of bilateral renal ischemia/reperfusion (I/R) injury and were sacrificed at the indicated time points. (A) Blood urea nitrogen (BUN) and serum creatinine levels in WT and MΦ atg5^−/− mice at days 0, 1, 4, and 7 after I/R injury (n = 8–10 per group). (B and C) Flow cytometric analysis showing the number of renal macrophages (F4/80⁺ CD11b⁺ CD11c⁻ CD45⁺ cells) in MΦ atg5^−/− and WT mice (B) at baseline and (C) on days 1 and 4 after I/R. Data are presented as the mean ± SEM, * P < 0.05, ** P < 0.01 (n = 3–4 per group). (D) Immunohistochemical staining for CD11b on kidney sections from both experimental groups at days 1 and 4 after AKI induction. Scale bar: 50 μm. Quantitation of the levels of CD11b⁺ cells from the renal cortex of MΦ atg5^−/− and WT mice. Data are presented as the mean ± SEM, **** P < 0.0001 (n = 4 per group). One-way ANOVA with Tukey’s multiple-comparison test (A, C, D); Unpaired, two-tailed Student’s t test (B)