P.g induces ferroptosis in the kidney in vivo andin vitro.
ACSL4 was upregulated, and xCT and GPX4 were downregulated in the kidney tissue of mice in the P.g group, as shown by IHC (Fig. 5A-C) and Western blotting (Fig. 5D, Supplementary Figure 3A). RT‒PCR indicated that GPX4 was decreased and PTGS2 and NCOA4 were increased in the kidney in the P.g group (Fig. 5E). Furthermore, IF, Western blot and RT‒PCR analysis of GPX4, xCT and ACSL4 indicated that MΦCM effectively activated ferroptosis in GMCs in vitro (Fig. 5F-J, Supplementary Figure 3B), which showed the same trend as in vivo. This evidence confirmed that ferroptosis was activated in the kidney and GMCs byP.g administration.