Scar binding restricts molecular exchange

This proposed study asks why scar tissue can slow molecule movement across a healed wound even when its collagen fibre scaffold remains intact. The hypothesis places the brake in scar chemistry. Negatively charged sugar chains, called glycosaminoglycans, could temporarily cling to charged molecules and natural proteins, while same-size neutral tracers and water move more freely. A scar-like microfluidic channel, a small controlled-flow system, could test this. Restored protein exchange after verified binding-site modification, with collagen layout and wound strength preserved, would support chemical trapping. Cutting collagen bridges alone should leave restriction in place.