Figure 2.

Schematic representation of the relationship between telomere and CHIP in atherogenesis. Risk factors (e.g., age, smoking, environmental exposures) influence the occurrence of a mutation in a CHIP driver gene of hematopoietic stem cells (HSCs), resulting in the expansion of a mutated HSC clone and mutant circulating leukocytes. The clonal expansion can promote inflammation and intensify telomere shortening in arteries, which further accelerates the adverse effects of telomere dysfunction on the vascular cell senescence and dysfunction, contributing to plaque formation and atherothrombotic risk.