ArticleBiology direct2026
FOSL1 upregulation contributes to ischemia/reperfusion-induced acute kidney injury by regulating GPX4-dependent ferroptosis.
Article in Biology direct, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
- MACC1 in colorectal cancer: a claim-level evidence audit from metastasis driver to proposed microenvironmental regulator.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026Review
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Authors and funding
4 authors.
Funding
Abstract
Fos-like antigen 1 (FOSL1) has been implicated in the pathology of acute kidney injury (AKI), but its specific mechanism remains unclear. In this study, we investigated the role of FOSL1 in the regulation of ferroptosis and inflammation in the context of ischemia-reperfusion (I/R)-induced AKI. Our results showed that renal I/R resulted in renal injury as evidenced by renal tissue damage and decreased renal function accompanied by increased FOSL1 expression, all of which was effectively restored by FOSL1 knockout (KO) in mice. FOSL1 KO downregulated the levels of pro-inflammatory cytokines and the number of CD4
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