Cd24a, encoding the mucin-like GPI-linked membrane protein CD24, is involved in multiple biological processes. It has been associated with cell-fate determination, immune response regulation, and tissue homeostasis [2,3]. In the immune system, it helps distinguish between danger-and pathogen-associated molecular patterns [2]. It also serves as a marker for certain stem cell populations, like multipotent dental pulp regenerative stem cells (MDPSCs), indicating its role in tissue regeneration [3].

In a murine model of acute kidney injury (AKI), AKI induced proximal tubule dedifferentiation with a pronounced nephrogenic signature represented by Cd24a [1]. In aged Cd24a null mice, the lens develops normally until 2 months of age but then shows abnormal fiber cell structure, actin filament disorganization, and refractive defects leading to premature cataract development by 1 year, suggesting its role in maintaining lens transparency [5]. In hepatocellular carcinoma (HCC), CD24A (an isoform of CD24) promotes cell proliferation, migration, and invasion, and is downregulated by EGR1 [6]. In acute lung injury, activated neutrophils have lower expression of Cd24a, while aged neutrophils have higher expression, and mesenchymal stem cell treatment can shift activated neutrophils towards an aged phenotype by upregulating CD24 [4].

In conclusion, Cd24a is essential for various biological functions including tissue development, immune response, and tissue repair. Studies using gene-knockout mouse models, like those for the lens and in AKI, have revealed its significance in maintaining tissue integrity and in the context of disease-associated processes such as cataract development, kidney injury, and cancer progression.