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. Author manuscript; available in PMC: 2021 Oct 1.
Published in final edited form as: J Cardiovasc Transl Res. 2020 Jan 6;13(5):686–701. doi: 10.1007/s12265-019-09952-8

Table 3:

The cellular and biochemical events associated with reparative, proliferative and maturation phases of the remodeling of IZ following MI.

Reparative and proliferative phase
Biochemical
events
Pathological effects References
Suppression of inflammation Decrease in pro-inflammatory cytokines, hypoxia, acidosis and neutrophil density and increase in anti-inflammatory cytokines, M2 macrophages, lipid-derived pro-resolving mediators and pro-fibrosis mediators [11]
Fibroblast activation and scarring Transdifferentiation of cardiac fibroblasts to the synthetic phenotype called myofibroblast [22]
ECM
remodeling
Formation of mechanically weak provisional matrix comprising fibrin and fibronectin is formed at IZ which matures by collagen deposition [23]
Maturation phase
Biochemical
events
Pathological effects References
Scar maturation ECM cross linking, deactivation of reparative cells, withdrawal of fibrogenic growth factors, clearance of matricellular proteins, and reduction in ECM synthesis and myofibroblast density [24]