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Microglial RUNX1/RBM47 ablation inhibits neuronal ferroptosis via regulating the cGAS-STING-MEF2C pathway in mice
Shanshan Wang1, Zankai Wu2, Wenqin Song1
1Department of Anesthesiology, Renmin Hospital of Wuhan University, Wuhan, China.
Communications Biology
|December 17, 2025
Summary
Repressing RUNX1 and RBM47 may offer a new treatment for postoperative cognitive dysfunction (POCD). This study reveals how RBM47 regulates the cGAS-STING pathway, impacting neuronal ferroptosis and POCD development.
Area of Science:
- Neuroscience
- Immunology
- Molecular Biology
Background:
- Postoperative cognitive dysfunction (POCD) is linked to cGAS-STING pathway activation.
- Rbm47 is upregulated in experimental POCD models, suggesting its involvement.
Purpose of the Study:
- To investigate the role of Rbm47 in the cGAS-STING pathway and its contribution to POCD.
- To explore the therapeutic potential of targeting the RUNX1/RBM47 axis for POCD treatment.
Main Methods:
- Analysis of transcriptomic data from mouse hippocampus.
- In vitro experiments using BV2 and HT22 cell lines with Rbm47 knockdown (KD) and overexpression.
- In vivo studies involving Rbm47 KD and cGAS inhibitor (RU.521) treatment in male mice.
- Investigation of the molecular interaction between RBM47 and cGAS mRNA, and RUNX1 binding to the Rbm47 promoter.
Main Results:
- Rbm47 KD reduced cGAS-STING pathway activation and inflammatory cytokine production in vitro.
- Rbm47 KD or cGAS inhibition ameliorated POCD symptoms in mice.
- RBM47 stabilizes cGAS mRNA, and RUNX1 promotes Rbm47 transcription.
- RUNX1 overexpression exacerbated POCD and ferroptosis, while RUNX1 ablation had protective effects.
Conclusions:
- The RUNX1/RBM47 axis is a key regulator of the cGAS-STING pathway and neuronal ferroptosis in POCD.
- Targeting RUNX1/RBM47 presents a promising therapeutic strategy for preventing and treating POCD.
