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. 2024 Jun 12;137(14):1651–1662. doi: 10.1097/CM9.0000000000003169

Figure 3.

Figure 3

The molecular mechanism of ferroptosis exacerbating OA and potential therapeutic targets. Ferroptosis of articular chondrocytes is associated with the pathogenesis of OA. The pathways and networks through which ferroptosis regulates the progression of OA can be divided into four basic categories, specifically amino acid metabolism (blue background section), lipid metabolism (green background section), iron metabolism (red background section), and others (yellow background section). The red font indicates potential therapeutic drugs or reagents. The data cut-off date for the analysis was February 1, 2024. AMPK: Adenosine 5′-monophosphate-activated protein kinase; CX43: Connexin 43; DFO: Deferoxamine; DMT1: Divalent metal transporter 1; FOXO3: Forkhead box O3; FPN1: Ferroportin; GPX4: Glutathione peroxidase 4; GSH: Glutathione; HIF-1α: Hypoxia-inducible factor-1 alpha; HIF-2α: Hypoxia-inducible factor-2 alpha; HMOX1: Heme oxygenase 1; HSPA5: Heat shock protein family a member 5; JNK: C-Jun N-terminal kinase; LIP: Labile iron pool; MAPK: Mitogen-activated protein kinase; NCOA4: Nuclear receptor coactivator 4; NF-κB: Nuclear factor kappa B; NRF2: Nuclear factor erythroid 2-related factor 2; OA: Osteoarthritis; SCP2: Sterol carrier protein 2; SIRT1: Silent mating type information regulation 2 homolog-1; SLC2A1: Solute carrier family 2 member 1; SLC3A2: Solute carrier family 3 member 2; SLC7A11: Solute carrier family 7 member 11; SND1: Staphylococcal nuclease domain containing 1; SREBF2: Sterol regulatory element binding transcription factor 2; STEAP3: Six-transmembrane epithelial antigen of the prostate 3; TF: Transferrin; TF3: Theaflavin-3,3′-digallate; TFR1: Transferrin receptor 1; TGF-β1: Transforming growth factor-beta 1; TRPV1: Transient receptor potential vanilloid 1; YAP1: Yes-associated protein 1.