Figure 1.

Probable mechanism of cardiovascular injury associated with clonal hematopoiesis. Mutant HSC-derived monocytes circulate and are recruited to plaques in arteries. There, they differentiate into tissue macrophages, which promote inflammation. The inflammasome activates IL-1β, which, in turn, promotes local inflammation, accelerating atherosclerosis, as well as induces expression of the P-selectin glycoprotein, which, in turn, recruits more monocytes (clonally derived and wild-type). Clonally derived platelets may also play an important role. In addition, increased interleukin-1β secretion in endothelial cells within the myocardium promotes disordered remodeling that potentiates heart failure.