Nt5e, also known as CD73, encodes an ecto-5'-nucleotidase expressed on the cell surface of various cell types. It hydrolyzes extracellular adenosine monophosphate into adenosine and inorganic phosphate, performing numerous homeostatic functions in healthy organs and tissues. It is associated with the p53 signaling pathway, which regulates cell senescence [1]. NT5E can act as an inhibitory immune checkpoint molecule, and its expression can influence immune responses and tumor cell immune escape [2].

In a mouse model of alcohol-related liver fibrosis (ALF), the absence of Nt5e was protective. Mechanistically, Nt5e regulated ALF and the activation and senescence of stellate cells by binding to AURKA, inhibiting AURKA ubiquitination and downregulating p53 signaling [1].

In conclusion, Nt5e is involved in multiple biological processes, and its absence in KO mouse models has revealed its role in alcohol-related liver fibrosis, suggesting it could be a potential therapeutic target for this disease. Its functions in immune regulation and cell senescence-related pathways also highlight its importance in understanding disease mechanisms [1,2].