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. 2022 Feb 17;10(3):877–890. doi: 10.1016/j.gendis.2021.12.023

Figure 4.

Fig. 4

The role and mechanism of CDO1 in physiological processes. CDO1 can promote cysteine metabolism, and then reduce the synthesis of GSH, leading to oxidative stress. Similarly, cysteine decomposition leads to decreased H2S synthesis and promotes mitochondrial function. CDO1 can promote the production of taurine, which can improve fertility and promote bile acid metabolism, and CDO1-mediated sulfate metabolism also plays an important role in fertility. In addition, CDO1 can significantly promote the expression of adipocyte differentiation-related genes, including PPARγ, C/EBPα and Fabp4, thereby facilitating adipogenesis. Cdo1 may regulate hepatic lipid metabolism by regulating FAO. CDO1 is a negative regulator of osteogenesis. It can inhibit the expression of osteogenic related genes, such as ColIa1 and Tbsp, and CDO1 inhibits Wnt signaling and restricts Wnt-induced expression of osteogenic transcriptional factors in BMSC, such as Runx2 and Dlx5. BMSC, bone marrow-derived mesenchymal stem cells; C/EBPα, CCAAT/enhancer-binding protein α; ColIa1, collagen, type I, alpha 1; Dlx5, distal-less homeobox 5; Fabp4, fatty acid binding protein-4; FAO, fatty acid oxidation; PPARγ, peroxisome proliferator-activated receptor γ; Runx2, runt-related transcription factor 2; Tbsp integrin binding sialoprotein.