Single-cell transcriptomics identifies potential roles of CCL2-mediated macrophage-endothelial cell interactions in endothelial apoptosis of varicose veins.

BACKGROUND: Varicose veins represent a prevalent vascular disorder. Both varicose veins and their associated complications can result in diminished quality of life, reduced work productivity due to lost working days, and escalating medical costs. The etiology of this condition is multifactorial. Despite notable advancements in varicose vein research in recent years, the precise molecular mechanisms underlying the disease remain incompletely elucidated.

METHODS: Researchers collected samples of varicose saphenous veins resected by vein stripping and normal saphenous veins obtained during coronary artery bypass graft surgery, and systematically resolved cellular heterogeneity, cell-cell interactions, and differentiation trajectories in the samples by using single-cell transcriptome sequencing (scRNA-seq) technology.

RESULTS: Endothelial cells and macrophages play a key role in pathological tissue remodeling associated with varicose veins. Endothelial cell apoptosis was observed in the study, while the interaction between CCL2-expressing macrophages and endothelial cells may trigger endothelial cell activation, immune cell recruitment, and increased vascular inflammation, which in turn disrupts the integrity and function of the endothelial barrier and contributes to varicose vein development and progression.

CONCLUSION: This study reveals cellular heterogeneity and its interactions in varicose veins of the lower extremities, and the interactions between specific cellular subpopulations provide a theoretical basis for the development of novel therapeutic targets, which are expected to interrupt the vicious cycle of inflammation and vascular injury in varicose veins.