Controlled inflammation has become a central focus in chronic disease therapeutics. Exaggerated inflammation is a common factor that contributes to matrix destruction, cellular senescence, and nonhealing in a variety of disease processes.

Efforts at controlling inflammation have traditionally concentrated on systemic antagonists to inflammation such as nonsteroidal anti-inflammatory agents. More recently, following increased appreciation of local biological cellular and molecular events occurring at the wound interface, efforts are being focused on local targeted approaches to catabasis, the resolution of inflammation.

These efforts relate to the isolation and understanding of the mechanisms of actions of various "stop signal mediators." These lipoxins, resolvins, and protectins are produced and stimulated by cellular interactions in the blood stream, extracellular matrix, and in cells themselves. Transmission of these signals between cells and the extracellular matrix and between cells themselves occurs via a variety of mechanisms including through intracellular gap junctions, connexins, and cadherins. The existence of these mediators, signals, and channels of communication all provide new therapeutic options for achieving catabasis in a more defined and targeted fashion.