Myofibroblasts are rich in F-actin bundles, which establish cell-cell and cell-matrix linkages and thus generate the force for wound contraction.

Fragmentation of fibronectin by proteases has been suggested to promote wound contraction, a critical step in wound healing.

The proliferative phase is characterized by angiogenesis, collagen deposition, granulation tissue formation, epithelialization, and wound contraction.

In addition to providing support for fibroblast and endothelial cell attachment, biodegradable scaffolds inhibit wound contraction, thereby allowing the healing process to proceed towards a more-regenerative/less-scarring pathway.

Moist wound therapy is known to promote fibroblast and keratinocyte proliferation and migration, collagen synthesis, early angiogenesis and wound contraction.

Fibroblasts from diabetic ulcer exhibit proliferative impairment that probably contributes to a decreased production of extracellular matrix proteins and delayed wound contraction and impaired wound healing.

This gel may then be allowed to contract as a model of wound contraction.

The collagen gel contraction assay is a type of wound contraction.

In the dermal wounds of rabbits GHK-Cu facilitated wound healing, causing better wound contraction, faster development of granular tissue and improved angiogenesis.

This GHK-Cu enriched material stimulated wound contraction and cell proliferation, as well as increased expression of antioxidant enzymes.