GEO series
PPARγ-Mediated Ferroptosis in Macrophages Enhances Persistent Pulmonary Infction by Mycobacterium tuberculosis
GSE275146
Mus musculus
Genome binding/occupancy profiling by high throughput sequencing; Other
16 samples
2026/04/24
GPL24247GPL30172
Summary
In this study, we found that Mycobacterium tuberculosis (Mtb) uses the PPARγ-GPX4 axis to induce ferroptosis in host cells, promoting persistent infection. Elevated PPARγ levels in macrophages post-Mtb infection, due to direct interactions with Mtb IDH and impaired degradation, lead to suppressed GPX4 expression and increased lipid peroxidation. Deleting PPARγ reduces lung inflammation, Mtb burden, and restores GPX4 expression in infected macrophages. This discovery of Mtb hijacking PPARγ to induce ferroptosis suggests a promising target for tuberculosis treatment.
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Paper (PMID 42259813) ↗
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