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.