STOmics technology:BGI Stereomics Stereo-Seq

Data type:Spatial transcriptomics

Sample scope:Multiisolate

Summary:Advanced atherosclerosis (AS) is the dominant cause of cardiovascular and cerebrovascular events. Tumors may occur during the progression of advanced AS. However, the effect of new-onset tumors on advanced AS remains unclear. Our study demonstrated that individuals (patients and mice) with comorbid advanced AS and cancer exhibited decreased plaque size and enhanced plaque stability. Multiomics analysis revealed that tumors impede advanced AS progression by depriving arginine, suppressing T cell activation, and reducing the secretion of proinflammatory cytokines. Tumor-induced arginine deficiency disrupted the interaction between GPR137B and DDX3X, leading to the mitochondrial translocation of DDX3X. This translocation triggered T cell metabolic reprogramming and subsequent advanced AS suppression. These findings provide new insights into the impact of tumors on advanced AS and can guide the management of patients with coexisting conditions. This work also highlights the potential of targeting T cell GPR137B deletion as a therapeutic strategy for atherosclerotic diseases.

Contributor(s):Yue Wang.

Submitter:李青松(Qingsong Li),BGI

Release date:2026-04-01

Updated:2026-04-01