Table 3 Mechanisms of mitochondrial and metabolic dysfunction that affect monocyte functions
From: Mitochondrial and metabolic dysfunction of peripheral immune cells in multiple sclerosis
Mechanism of mitochondrial and metabolic dysfunction | Monocytes functions | References |
|---|---|---|
The inhibitor 6877002 decreases ROS production of monocytes through CD40-TRAF6 pathway | Reduce pro-inflammatory cytokines (TNF, IL-6) production and trans-endothelial migration ability | [115] |
2-DG treatment reduces glucose uptake, lactate secretion and ECAR in monocytes, which was correlated with a decrease in the expression of Glut1, HK-2, TPI, PKM, LDHA, and MCT-1 | Switch to an anti-inflammatory phenotype and 2-DG treated monocytes attenuate the severity of experimental autoimmune encephalomyelitis (EAE) | [114] |
DMF treatment increases ROS production in monocytes, which was correlated with genetic variation and CpG methylation in monocytic NOX3 | Increase the numbers of monocytes | [120] |
IFN-beta treatment alters mitochondrial dysfunction pathway and mitochondrial ETC-related genes | Decrease monocytic ROS production |