Collagen fibril formation. A new target to limit fibrosis.

This article details a potentially exciting new therapeutic target that is designed to prevent or impede the development of scar tissue which occurs following injury and/or inflammation.

Specifically, the authors demonstrate that monoclonal antibodies against the extracellular matrix protein collagen I, a major structural component of fibrotic scars, not only inhibit collagen fibril formation in vitro but decrease the density of collagen fibrils in a model of fibrosis in the skin of mice.

Collagen molecules assemble into higher order structures via the interaction of the telopeptide of one collagen with a region of the triple helix of another collagen. The monoclonal antibodies used in this study block this interaction and thereby inhibit collagen fibril assembly. Their use following surgery might not only provide a more cosmetically pleasing outcome by blocking assembly of keloids but should reduce those fibrotic reactions that lead to interference in normal tissue function. Clinical applications will require that the antibodies be humanized and further work will be required to demonstrate whether this approach has utility in limiting systemic fibrotic disease.