Ido1, short for Indoleamine 2,3-dioxygenase 1, is a rate-limiting metabolic enzyme. It catalyzes the initial step of the kynurenine (KYN) metabolic pathway by converting the essential amino acid tryptophan into kynurenine. This pathway is associated with multiple processes, such as de novo NAD+ biosynthesis, 1-carbon metabolism, and activation of the aryl hydrocarbon receptor (AhR). Ido1 is involved in important biological functions like immune regulation, with its expression promoting immune tolerance, and it has a significant impact on tumor-promoting inflammation, neovascularization, and the aging process [1,2,3].

In cancer, while single-agent treatment with Ido1 enzyme inhibitor has shown negligible effects on reducing cancer burden, combinations with other therapies tend to yield synergistic benefits against tumor growth [5]. In liver fibrosis, the compound corilagin alleviates fibrosis by repressing Ido1-mediated M2 macrophage repolarization [4]. In the context of the aging process, Ido1 activation in chronic inflammatory states stimulates the KYN pathway, which has harmful effects such as immunosuppression, impaired autophagy, and enhanced development of osteoporosis and vascular diseases [2].

In conclusion, Ido1 is a key enzyme in the tryptophan-kynurenine metabolic pathway, playing important roles in immune regulation, cancer development, and the aging process. Studies on Ido1, including those using potential gene-knockout or conditional-knockout mouse models, help us understand its functions in these biological processes and disease conditions, potentially providing new strategies for treating related diseases.