ADK, short for adenosine kinase, is crucial in the purine salvage pathway, converting adenosine to AMP. It also regulates methylation reactions. ADK's function is associated with multiple pathways, such as those related to inflammation, energy metabolism, and neurotransmission, and is of great biological importance in maintaining normal physiological functions [2,4]. Genetic models, like KO/CKO mouse models, are valuable tools for studying ADK.

In depression, Hyperibone J, a component from Hypericum bellum, binds to ADK at the ASN-312 site, reducing its stability and expression, thus inhibiting microglial P2X7R/TLR4-mediated neuroinflammation and alleviating depression-like behaviors [1]. In non-alcoholic fatty liver disease, hepatocyte-specific ADK disruption in mice decreases hepatic fat deposition and protects against diet-induced excessive fat deposition and inflammation, while overexpression promotes these adverse effects [2]. In nerve damage repair, ADK suppresses injured neurite re-growth, and the application of its inhibitor 5-Iodotubercidin enhances motor function recovery in mice with spinal cord injury [3].

In conclusion, ADK plays key roles in various biological processes. Model-based research, especially using KO/CKO mouse models, has revealed its significance in diseases like depression, non-alcoholic fatty liver disease, and nerve damage. Understanding ADK's functions provides insights into the mechanisms of these diseases and potential therapeutic targets.