ZFYVE28, also known as LST2, contains a FYVE domain and is involved in multiple biological functions and pathways. It plays a role in endosomal regulation, specifically in the conversion of early to late endosomes, and is associated with signaling pathways such as the insulin signaling pathway, EGFR-signaling pathway, and mTORC1-related pathways [1,2,3]. It may also be involved in processes related to sleep, vesicle-mediated transport, and is potentially associated with diseases like insulin resistance, glomerular diseases, intellectual disability, psoriasis, and polycystic ovary syndrome [1-3,5,8].

In insulin-related research, Zfyve28 knockout in mice significantly improves insulin sensitivity and other insulin-resistance-associated indicators. It promotes phosphorylated insulin receptor degradation by increasing late endosomes production, and its expression is regulated by insulin signaling [1]. In podocytes, ZFYVE28 is a podocyte-enriched gene. Although ZFYVE28-deficient mice have normal kidney development and maintenance of the filtration barrier, overexpression of ZFYVE28 in cultured podocytes promotes EGF-signaling, possibly by up-regulating EGFR expression and modulating its localization [2].

In conclusion, ZFYVE28 is an important gene involved in endosomal regulation and multiple signaling pathways. Gene knockout mouse models have revealed its role in insulin resistance and podocyte EGF-signaling. Understanding ZFYVE28's functions may provide potential therapeutic targets for related diseases such as insulin resistance and psoriasis [1,2,4].