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MFN2 and BAG6 Synergistically Protect Against Cerebral Reperfusion Injury by Regulating ROS Levels and Autophagic

Dongting Lu1, Yukun Yang2, Guodong Huang3

  • 1Department of Neurology, Guangxi University of Chinese Medicine, Nanning, China (D.L., Y.-C.W.).

Stroke
|September 2, 2025
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Summary

Mitofusin-2 (MFN2) protects against stroke by reducing reactive oxygen species (ROS) and modulating autophagy through interaction with BAG6. This MFN2-BAG6 axis offers a promising therapeutic target for stroke treatment.

Keywords:
autophagyglucoseinfarction, middle cerebral arteryischemic stroketriphenyltetrazolium

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Area of Science:

  • Neuroscience
  • Cell Biology
  • Mitochondrial Biology

Background:

  • Mitofusin-2 (MFN2) is a mitochondrial outer membrane protein crucial for mitochondrial fusion and autophagy.
  • In vitro studies suggest MFN2 possesses neuroprotective properties following ischemic events.
  • This study investigates MFN2's role in neuronal ischemia/reperfusion injury in vivo and in vitro.

Purpose of the Study:

  • To elucidate the role of MFN2 in neuronal ischemia/reperfusion injury.
  • To investigate the mechanisms by which MFN2 exerts neuroprotection.
  • To explore the interaction between MFN2 and its partner BAG6 in the context of stroke.

Main Methods:

  • MFN2 was manipulated (knockdown/overexpression) in mice and neuronal cells subjected to ischemia/reperfusion models.
  • Neurological deficits, infarct volume, apoptosis, necrosis, ROS levels, and autophagic flux were assessed.
  • Protein interactions were analyzed using immunoprecipitation, mass spectrometry, and Western blotting.

Main Results:

  • Neuron-specific MFN2 deletion worsened ischemia/reperfusion injury, while MFN2 overexpression improved outcomes.
  • MFN2 deficiency increased mitochondrial ROS and inhibited autophagy; MFN2 overexpression decreased ROS and modulated autophagy.
  • A direct interaction between MFN2 and BAG6 was identified, with BAG6 overexpression mimicking MFN2's protective effects.

Conclusions:

  • MFN2 enhances stroke outcomes by reducing ROS and modulating autophagy via interaction with BAG6.
  • BAG6 amplifies MFN2's ROS-lowering and cytoprotective actions.
  • The MFN2-BAG6 axis presents a potential therapeutic strategy for stroke.