Aox1, or aldehyde oxidase 1, has diverse functions. It is involved in retinol metabolism [1]. In addition, it has been associated with pathways related to osteoblastogenesis in human periodontal ligament stem cells (hPDLMSCs), where its expression is upregulated during osteoinduction [2].

In liver fibrosis, knockout of Sema4D alleviates liver fibrosis by suppressing AOX1 expression in retinol metabolism. This shows that AOX1 is involved in the pathological process of liver fibrosis [1]. In hPDLMSCs, AOX1 silencing enhances the osteogenic potential, indicating its role in negatively regulating osteogenesis [2]. In clear cell renal cell carcinoma (ccRCC), lower AOX1 expression was found in cancer tissues compared to normal tissues, and higher AOX1 expression predicted better overall survival, suggesting it may act as a tumor suppressor gene [3]. In prostate cancer, AOX1 was lowly expressed and hypermethylated, and knocking down AOX1 promoted cell migration and invasion, suggesting its potential as a biomarker [4]. In pediatric papillary thyroid carcinoma, AOX1 expression was downregulated, and low levels were associated with poor survival, indicating its potential as a biomarker for diagnosis and prognosis [5]. In human mesenchymal stem cells, AOX1 was identified as an osteogenic differentiation-relevant gene, and its overexpression increased the expression of osteo-specific genes [6].

In summary, Aox1 plays important roles in various biological processes and disease conditions. Studies using gene knockout or knockdown models have revealed its significance in liver fibrosis, osteogenesis, and multiple types of cancers, providing insights into disease mechanisms and potential biomarker discovery.