The Contributive Role of IGFBP-3 and Mitochondria in Synoviocyte-Induced Osteoarthritis through Hypoxia/Reoxygenation Injury: A Pathogenesis-Focused Literature Review

Figure 2

Involvement of the synovial membrane in OA pathophysiology (reprinted from Sellam and Berenbaum [4] and reused with permission from Nature Springer under license no. 4820091329692). The type A synoviocytes phagocytosed the cartilage breakdown products that are released into the synovial fluid, amplifying synovitis. This process will lead to the production of anti-inflammatory substance and to the formation of osteophytes via the bone morphogenetic protein (BMP). Abbreviations: CCL2: CC-chemokine ligand 2; CXCL13: CXC-chemokine ligand 13; EGF: endothelial growth factor; GM-CSF: granulocyte-macrophage colony-stimulating factor; IL-1Ra: IL-1 receptor antagonist; LIF: leukemia inhibitory factor; LTB4: leukotriene B4; NAMPT: nicotinamide phosphoribosyl transferase; NO: nitric oxide; NGF: nerve growth factor; PGE2: prostaglandin E2; TIMP: tissue inhibitor of metalloproteinase; TNF: tumor necrosis factor; VCAM-1: vascular cell adhesion molecule 1; VEGF: vascular endothelial growth factor.