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Once produced, TMAO is oxidized in the liver by flavin-containing monooxygenase 3 (FMO3), and has emerged as a key contributor to atherosclerosis and other cardiovascular diseases (CVDs) [1]

doi: 10.1016/B978-0-12-381272-8.00001-5

By integrating these findings, this review offers new insights into the role of ferroptosis in joint degeneration and highlights its potential as a therapeutic target in osteoarthritis