ADAM10, a member of the ADAM superfamily, is a membrane-bound zinc-dependent protease with its catalytic domain on the cell surface. It functions as a sheddase, cleaving over 100 different anchored cell-surface proteins. ADAM10 is involved in multiple key pathways, most notably Notch signaling, and is crucial for mammalian development, physiology, and tissue homeostasis [2,3].

In hair follicles, ablation of the ADAM10-Notch signaling axis in mice impaired the innate epithelial barrier, caused skin dysbiosis, and led to hair follicle destruction due to group 2 innate lymphoid cell-mediated inflammation [5]. In renal diseases, ADAM10 is associated with the progress of glomerular diseases, acute kidney injury, and renal fibrosis, and its catalytic action on kidney-related molecules like Notch is significant [1]. In cancer, ADAM10 cleavage of Trop-2 acts as an activator switch for cancer growth and metastasis, and it also modulates the efficacy of T-cell-mediated therapy in solid tumors [6,7]. In sepsis, ADAM10 acts as a “molecular scissor” regulating proteolysis during the inflammatory response [4].

In conclusion, ADAM10 is essential for numerous biological processes through its sheddase activity and involvement in key signaling pathways. Studies using gene-knockout or conditional-knockout mouse models have revealed its role in diseases such as skin disorders, renal diseases, cancer, and sepsis. Understanding ADAM10's functions provides potential therapeutic targets for these disease areas.