Txnip, also known as thioredoxin interacting protein or VDUP1 (vitamin D3 upregulated protein-1), is an alpha-arrestin protein crucial for redox homeostasis in the human body. It binds to thioredoxin (TRX) to inhibit TRX function and expression, and is involved in multiple pathways such as those related to glucose and lipid metabolism, cell cycle arrest, and inflammation [3,4].

In non-alcoholic steatohepatitis (NASH), deletion of the Txnip gene in mice enhanced hepatic steatosis, inflammation, and fibrosis, accompanied by impaired autophagy and fatty acid oxidation (FAO) [1]. In atherosclerotic calcification, Txnip-/-mice presented increased calcification and collagen deposition, with an expanded osteochondrogenic cluster derived from VSMCs [2]. In diabetic kidney disease, Txnip knockout suppressed renal fibrosis and mTORC1 activation, while restoring TFEB and autophagy activation in diabetic kidneys [5].

In conclusion, Txnip plays essential roles in maintaining redox balance and regulating various biological processes. Gene knockout mouse models have revealed its significance in diseases like NASH, atherosclerotic calcification, and diabetic kidney disease, providing valuable insights into potential therapeutic strategies targeting Txnip for these conditions.