ArticleCommunications biology2025
Biphasic protective effects of macrophage migration inhibitory factor in ischemia/reperfusion-induced acute kidney injury.
Article in Communications biology, 2025. 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.
- Molecular mechanisms of macrophage migration inhibitory factor in related diseases (Review).Biomedical reports · 2026Review
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ferroptosis is involved in the occurrence and progression of renal ischemia/reperfusion (I/R) injury. Macrophage migration inhibitory factor (MIF) is a pleiotropic cytokine that is closely associated with kidney diseases. However, the underlying mechanisms between MIF and ferroptosis in acute kidney injury (AKI) still remain unclear. In contrast to conventional strategies, we further investigate the dynamic expression and role of MIF in both ischemic and reperfusion phases. In the present study, we establish hypoxia/reoxygenation (H/R) and I/R induced AKI models, verify ferroptosis by detecting pro-ferroptotic changes and associated indicators, and use si-RNA or Adeno-Associated virus (AAV) to knock down the expression of MIF, observing subsequent changes of ferroptosis. The results show that treatment with recombinant MIF reduces lipid ROS generation and MDA levels, upregulating glutathione (GSH) levels, with increasing AMP-activated protein kinase (AMPK) phosphorylation. While the deficiency of MIF blunted its protective effect on renal tubular epithelial cells, which demonstrates that MIF ameliorates ferroptosis injury via activating the AMPK pathway in the ischemia stage and increasing GSH content in the reperfusion stage. In conclusion, our results suggest the nephroprotective role of MIF in inhibiting ferroptosis and provide insight into the prevention and treatment of AKI.
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