Fig. 3: Deletion of Otud5 renders kidneys vulnerable to I/R.
From: Autophagy of OTUD5 destabilizes GPX4 to confer ferroptosis-dependent kidney injury
a The schematic shows the crossing of Pax8-Cre mice and Otud5-floxed mice to generate renal tubular cell conditional Otud5 knockout (Pax8CreOtud5fl/fl) mice. b 4–6-week-old Pax8CreOtud5fl/fl mice and their WT littermates (n = 5) were subjected to kidney I/R surgery. After 48 h, kidneys were collected and subjected to H&E, IHC staining, immunofluorescence analysis, TUNEL staining and quantification for kidney injury score evaluation, GPX4 and 4-HNE expression, F4/80 expression, and cell death, respectively; Scale bars, 50 μm. The asterisk indicates the injured tubular area. a.u.: arbitrary units. c–h Bar plots show the BUN (c), SCr levels (d), and mRNA level of kidney injury markers Lcn (e) and Havcr1 (f) Il6 (g), and Tnf (h) of Pax8CreOtud5fl/fl mice and their WT littermates in response to I/R. All values are presented as mean ± s.e.m., n = 5; p values were calculated by unpaired two-tailed Student’s t-test.
