Figure 3.

Schematic illustration of the process of fibrotic scar formation at the cellular level. The myocardium develops cardiomyocyte hypertrophy under pressure overload conditions, triggering concomitant inflammatory processes and fibrotic scar formation. The evidence discussed in the text suggests a central role for resident fibroblasts, nonetheless cardiac endothelial cells may also contribute to myofibroblast-like cells and drive cardiac fibrosis. Resident and infiltrating immune cells, including mast cells, macrophages, and neutrophils, enhance this phenotype change by releasing TGFß while mediating tissue inflammation via cytokines such as TNFα, IL-6, and IL-1. These mechanisms increase the number of myofibroblasts and the accumulation of collagen, which accelerates fibrotic scar formation in the microenvironment of cardiac hypertrophy.