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Updated: Jun 11, 2025

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MEF2C Alleviates Postoperative Cognitive Dysfunction by Repressing Ferroptosis.

Shanshan Wang1, Zankai Wu2, Xueshan Bu1

  • 1Department of Anesthesiology, Renmin Hospital of Wuhan University, Wuhan, Hubei, China.

CNS Neuroscience & Therapeutics
|October 1, 2024
PubMed
Summary
This summary is machine-generated.

Myocyte-specific enhancer factor 2C (MEF2C) protects against postoperative cognitive dysfunction (POCD) by inhibiting ferroptosis. MEF2C overexpression improved memory and reduced cell damage, suggesting it as a therapeutic target for POCD.

Keywords:
ferroptosisglutathione peroxidase 4myocyte‐specific enhancer factor 2Cpostoperative cognitive dysfunction

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Area of Science:

  • Neuroscience
  • Cell Biology
  • Genetics

Background:

  • Postoperative cognitive dysfunction (POCD) is linked to ferroptosis, a cell death pathway involving lipid peroxidation.
  • Myocyte-specific enhancer factor 2C (MEF2C), a transcription factor, is involved in cognitive processes and brain function.
  • The role of MEF2C in POCD and its connection to ferroptosis remain unclear.

Purpose of the Study:

  • To investigate whether MEF2C influences cognitive function after surgery by modulating ferroptosis.
  • To explore the therapeutic potential of targeting MEF2C for preventing POCD.

Main Methods:

  • Transcriptomic analysis identified MEF2C as differentially expressed in POCD mouse hippocampus.
  • A POCD mouse model was created using anesthesia and surgery, with manipulated MEF2C and GPX4 inhibitor (RSL3) levels.
  • Cognitive function, cell damage markers, ferroptosis indicators, and MEF2C's transcriptional regulation of GPX4 were assessed.

Main Results:

  • MEF2C levels decreased in the hippocampus post-surgery and anesthesia.
  • Overexpressing MEF2C improved memory, reduced lipid peroxidation and iron accumulation, and boosted antioxidant capacity.
  • MEF2C directly activated GPX4 transcription by binding to its promoter, an effect reversed by RSL3.

Conclusions:

  • MEF2C plays a protective role against POCD by suppressing ferroptosis.
  • MEF2C's ability to transcriptionally activate GPX4 is key to its neuroprotective effects.
  • MEF2C represents a potential therapeutic target for mitigating POCD.