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Fig. 2 | Arthritis Research & Therapy

Fig. 2

From: The burden of metabolic syndrome on osteoarthritic joints

Fig. 2

Metabolic polarisation of macrophages. Circulating monocytes are recruited into the synovium whereby they differentiate into non-activated macrophages. Hyperglycaemia, insulin resistance, and pro-inflammatory cytokines inhibit AMPK activity resulting in HIF-1α stabilisation and increases in aerobic glycolysis. Increases in glycolysis are accompanied by increased PPP activity, and both are involved in M1 macrophage polarisation. Succinate stabilises HIF-1α. Citrate promotes aerobic glycolysis and inflammatory cytokine expression. Obesity and nutrient excess hyperactivate mTORC1 resulting in Akt inhibition and defective M2 polarisation. M2 polarisation is promoted by AMPK activity. AMPK is stimulated by nutrient deprivation, metformin, and adiponectin. Resolvin D1 promotes the re-polarisation of macrophages to the M1 phenotype. AMPK, 5′ adenosine monophosphate-activated protein kinase; HIF-1α, hypoxia-inducible factor alpha; PPP, pentose phosphate pathway; mTORC1, mammalian target of rapamycin complex 1; TNF-α, tumour necrosis factor alpha; MMP, matrix metalloproteinase; ROS, reactive oxygen species; IL, interleukin; TGF-β, transforming growth factor beta; VEGF, vascular endothelial growth factor. (A) CD11c, (B) CD14, (C) CD86, and (D) CD206

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