Table 4 Mechanisms of mitochondrial and metabolic dysfunction influence Mϕ functioning

DMF blocks the glycolysis process and ROS production by decreasing extracellular signal-regulated kinase (ERK) phosphorylation

Inhibit antigen-presenting function in Mϕ and switch to M2 phenotype

[124, 125]

FhHDM-1 upregulates oxidative phosphorylation (OXPHOS) and decreases glycolysis

Inhibit Mϕ activation and pro-inflammatory cytokines expression

[127, 128]

P47phox mediated ROS generation

Accumulate in infiltrating Mϕ and involved in demyelination

[133, 134]

Fibrin upregulates ROS production through enhancing oxidative stress genes (Ncf2, Sod2, Nox2) and p47phox

Promote activation of Mϕ and demyelination and axonal damage

[135, 136]

Deleting LDHA or MCT4 reduces lactate production

Inhibit pro-inflammatory Mϕ activity

[118]

Glycolysis upregulated in MHC-II⁺ Mϕ was associated with glucose transporters (GLUTs) and MCT-1

Promote MHC-II⁺ Mϕ activity in demyelination

[138]