Meox2, also known as Mesenchyme Homeobox 2, is a transcription factor involved in mesoderm differentiation, including the development of bones, muscles, vasculature, and dermatomes [4]. It has been associated with multiple signaling pathways such as ERK, PI3K/AKT, and is of great biological importance in various physiological and pathological processes [1,5,6]. Genetic models like mouse models are valuable for studying its functions.

In gliomas, Meox2 acts as an oncogenic transcription regulator, promoting cell proliferation, motility, and tumorigenesis. Knockdown of Meox2 in patient-derived GBM tumorspheres inhibited growth and altered ERK phosphorylation [1]. In glioma cells, its inhibition changed cell morphology, hindered epithelial-mesenchymal transition, focal adhesion formation, and F-actin assembly, while overexpression had opposite effects [2].

In DBA/2J glaucoma mouse models, Meox2 haploinsufficiency accelerated axonal degeneration, indicating its role in controlling IOP-dependent vascular remodeling and neuroinflammation to promote axon survival [3].

In hepatic stellate cells, overexpression of Meox2 inhibited cell vitality and proliferation by regulating the PI3K/AKT signaling pathway, thus slowing liver fibrosis progression [5].

In glioma stem-like cells, loss-of-function of Meox2 affected cell viability, proliferation, and adhesion through AKT/ERK pathways [6]. In glioblastoma stem cells, Meox2 knockdown inhibited cell growth, sphere-forming ability, and increased apoptosis, and it was involved in regulating genes of the glycolytic pathway and response to hypoxia [7].

In conclusion, Meox2 has diverse functions in mesoderm-related development and multiple disease conditions. Mouse models, especially those with Meox2 haploinsufficiency or knockdown, have been crucial in revealing its role in gliomas, glaucoma, and liver fibrosis. These findings provide insights into potential therapeutic targets for these diseases.