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. 2022 Jan 14;9:817104. doi: 10.3389/fcell.2021.817104

TABLE 1.

Cellular and molecular mechanisms underlying the interplay between iron overload and OA.

Osteoarthritic phenotypes Cells Mechanisms References
Cartilage degradation Chondrocytes Promote lipid peroxidation and stimulate ferroptosis Sun et al. (2020)
Mediate mitochondrial dysfunction through ROS production and oxidative stress response Jing et al. (2021a)
Subchondral bone destruction Osteoclasts Promote mitochondrial respiration and oxidative stress, and thus facilitate osteoclast differentiation Ishii et al. (2009)
Facilitate osteoclastogenesis by promoting the secretion of apoptotic osteocyte-derived RANKL Yang et al. (2020)
Osteoblasts Inhibit osteogenic differentiation of BMSCs through ROS-mediated Runx2 suppression Jing et al. (2019)
Induce osteoblast autophagy and apoptosis by upregulating the level of DMT1 Liu et al. (2017)
Promote osteoblast apoptosis by inducing ROS production and oxidative stress injury He et al. (2013)
Lead to G1 phase arrest and autophagy by inhibiting PI3K/AKT and JAK/STAT3 signaling and promoting p38 signaling Cen et al. (2018)
Synovitis Macrophages Induce M1 polarization by increasing ROS-stimulated p300/CBP acetyltransferase activity and p53 acetylation Zhou et al. (2018)
Neutrophils Promote the accumulation of neutrophils and regulate matrix-degrading enzymes production Heiland et al. (2010)
Fibroblast-like synoviocytes Promote cell proliferation by activating key genes c-myc and mdm2 Hakobyan et al. (2004)