Ogn, previously known as mimecan, belongs to the small leucine-rich proteoglycans family. It plays pivotal functions in tissue formation, damage response, and is involved in various biological processes such as cell proliferation, apoptosis, and differentiation. It is also associated with multiple signaling pathways including the TGF-β/Smad, PI3K/Akt/mTOR, and OGN-Hh pathways [1,2,3,4].

In the context of diseases, Ogn shows diverse roles. In pancreatic cancer, its up-regulation promotes tumorigenesis by targeting ID4 [1]. In lung fibrosis, Ogn up-regulation in lung myofibroblasts is involved in the pathogenesis, and its knockdown attenuates fibrosis by inhibiting integrin αv-mediated TGF-β/Smad pathway activation [2]. In breast cancer, Ogn functions as a tumor suppressor, inhibiting cell proliferation and invasiveness via the PI3K/Akt/mTOR pathway [4]. In the study of tooth root development, Ogn-/-mice showed accelerated root length growth rate and thicker root hard tissues, likely due to Hh pathway activation and increased cell proliferation and differentiation [3].

In conclusion, Ogn is a multifunctional gene involved in tissue development and disease processes. The use of Ogn-/-mouse models has provided valuable insights into its role in tooth root development. In disease areas, it has been shown to have both tumor-promoting and tumor-suppressing roles, depending on the cancer type, and is also implicated in fibrotic diseases, highlighting its potential as a biomarker and therapeutic target.