GOLM1, also known as GP73 or GOLPH2, is a Golgi-resident type 2 transmembrane protein. It is involved in multiple biological processes such as cytokine production, immune regulation, and lipid metabolism. It can affect the activation and degradation of intracellular signaling factors and is associated with pathways like TGFβ1/Smad2, EGFR-ERK, and ubiquitin-proteasome, playing an important role in various diseases [2,3,6,7]. Genetic models, especially KO/CKO mouse models, are valuable for studying GOLM1's functions.

In hepatocellular carcinoma, GOLM1 exacerbates CD8+ T cell suppression by promoting exosomal PD-L1 transport into tumor-associated macrophages [1]. In pulmonary fibrosis, GOLM1-knockout mice showed alleviated pulmonary fibrosis and collagen deposition, indicating that GOLM1 promotes pulmonary fibrosis through upregulation of NEAT1 [4]. In atherosclerosis, global deletion of GOLM1 in Apoe-/-mice ameliorated mouse inflammation and atherosclerosis, while knock-in exacerbated these manifestations. Hepatic GOLM1 deletion also reduced circulating GOLM1 and attenuated atherogenesis [5].

In conclusion, GOLM1 plays crucial roles in multiple diseases including cancer, pulmonary fibrosis, and atherosclerosis. The use of GOLM1 KO/CKO mouse models has significantly contributed to revealing its functions in these disease conditions, helping us understand its role in promoting disease progression and potentially providing new therapeutic targets.