Biomedical Engineering Reference
Disruption of native ECM architecture
Blood exposure to collagen leads to platelet
activation, clotting cascade initiation
Fibrin network is major clot component, stops
bleeding, closes the wound.
Cell proliferation and
Proliferating fibroblast create provisional fiber
network of collagen, fibronectin, hyaluronic acid.
HA facilitates cell migration and stimulates
endothelial cell proliferation. Fibronectin is involved
in re-epithelization and serves as template for
Wound tissue maturation;
ECM synthesis and
Initially randomly distributed collagen fibrils become
cross-linked, and aggregate into regularly organized
bundles oriented along the lines of stress in the
wound.Collagenases are involved in collagen
degradation and remodeling.
Wound contraction occurs as a result of an
interaction between fibroblast locomotion and
Collagen fibers impart stiffness and tensile strength
Block diagram of ECM remodeling in wound healing
endothelial cells all play a role in a well-established sequence of events that eventually
lead to repair of the damage tissue by remodeling ECM. In a schematic that divides
the wound healing into distinctive different stages (infl ammation, proliferation, and
remodeling; see Fig. 2 ), ECM remodeling in the wound begins as soon as a new
ECM is laid down. Different cell types play a key role at each stage and are regu-
lated by numerous growth factors and cytokines (Moore 2001 ) . The progression of
wound repair is frequently modeled in the skin, but parallel and temporally coordi-
nated events occur in most tissues following injury.