Fig. 9: A proposed model of MFN2-mediated regulation of innate immune responses during bacterial infection. | Communications Biology

Fig. 9: A proposed model of MFN2-mediated regulation of innate immune responses during bacterial infection.

From: Mitofusin-2 boosts innate immunity through the maintenance of aerobic glycolysis and activation of xenophagy in mice

Fig. 9

In response to mycobacterial or listerial infection, MFN2 is essentially required for antimicrobial host defense through immunometabolic remodeling and xenophagy activation. MFN2 contributes to the activation of inflammatory responses via the maintenance of aerobic glycolysis. During infection, MFN2 is crucial for the basal respiration of mitochondria and generation of mitochondrial ROS, which results in the HIF-1α expression and inflammatory signaling. In addition to immunometabolic regulation, MFN2 plays a role in the enhancement of xenophagic activation through interactions with Rab7.

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