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. Author manuscript; available in PMC: 2009 Aug 1.
Published in final edited form as: Pharmacol Res. 2008 Jun 24;58(2):88–111. doi: 10.1016/j.phrs.2008.06.007

Figure 1. Infarct healing is closely intertwined with ventricular remodeling.

Figure 1

The healing response can be divided in three overlapping phases. During the inflammatory phase, chemokines and cytokines are induced in the infarct and marked leukocyte infiltration is noted. Neutrophils and macrophages clear the wound from dead cells and matrix debris. During the proliferative phase of healing, activated macrophages release cytokines and growth factors leading to formation of highly-vascularized granulation tissue. At this stage expression of pro-inflammatory mediators is suppressed, while fibroblasts and endothelial cells proliferate. Activated myofibroblasts produce extracellular matrix proteins and an extensive microvascular network is formed. Maturation of the scar follows: fibroblasts and vascular cells undergo apoptosis and a collagen-based scar is formed. As the infarct heals, dilative remodeling of the infarcted ventricle is noted (top panel). The time course of the cellular events presented in this figure is based on a reperfused model of infarction in the mouse. Large animals and humans exhibit delayed healing in comparison with rodents.