Vcam1, known as Vascular cell adhesion molecule 1, belongs to the immunoglobulin superfamily of cell adhesion molecules. It plays a crucial role in mediating the strong adherence of leukocytes to endothelial cells, regulating inflammation, and facilitating leukocyte migration. It is involved in multiple pathways such as the AKT-mTOR-CXCL1 axis, and is of great biological importance in processes like immune response, cancer progression, and maintaining vascular integrity. Genetic models, like KO/CKO mouse models, are valuable tools for studying its functions.

In gastric cancer, H3K18 lactylation upregulates Vcam1 transcription, which activates AKT-mTOR signaling, promoting tumor cell proliferation, EMT transition, and metastasis. Vcam1 also upregulates CXCL1 expression via the AKT-mTOR pathway, facilitating the recruitment of hGC-MSCs and M2 macrophages [1]. In ovarian cancer, the VLA4/VCAM1 pathway in M2 macrophages is involved in regulating vascular permeability and ascites development. Targeting this axis can enhance vascular integrity and prevent ascites formation [2]. In sickle cell anemia, certain VCAM1 promoter haplotypes lead to higher VCAM1 expression, affecting systemic vasculopathy risk [3]. In liver fibrosis, VCAM1 expressed by liver sinusoidal endothelial cells promotes LSEC capillarization and liver fibrosis [4]. In chronic cerebral hypoperfusion, increased VCAM1 expression on brain endothelial cells drives blood-brain barrier impairment, and blocking VCAM1-mediated BBB impairment may be a new treatment strategy [5].

In conclusion, Vcam1 is essential in regulating inflammation, immune responses, and is closely associated with the progression of various diseases including cancer, ovarian ascites, sickle cell anemia-related vasculopathy, liver fibrosis, and chronic cerebral hypoperfusion-related neurodegenerative diseases. Studies using KO/CKO mouse models have significantly contributed to understanding its role in these disease conditions, providing potential therapeutic targets for treatment.