Cytokines are critical to a myriad of fundamental homeostatic and pathophysiological processes such as
fever, wound healing,
inflammation, tissue repair and
fibrosis. They play important roles in regulating cell function such as proliferation, migration, and matrix synthesis. It is the balance or the net effect of the complex interplay between these mediators, which appears to play a major role in regulating the initiation, progression and resolution of
wounds. Wound healing involves a complex process including induction of acute
inflammation by the initial injury, followed by parenchymal and mesenchymal cell proliferation, migration, and activation with production and deposition of extracellular matrix. Failure to resolve or abnormal wound healing results in
fibrosis. The latter process involves similar cellular interactions via complex
cytokine networks, which result in extensive remodeling with heightened extracellular matrix production and their abnormal deposition in the tissue. Various
cytokines, both promoting and inhibiting fibrogenesis, have been implicated in the pathogenesis of
fibrosis and wound healing. Recent progress in understanding the mechanisms underlying the pathogenesis of
fibrosis leads us to expect that inhibitors of pro-fibrogenic
cytokines and
growth factors may be useful as novel therapeutic agents in controlling undesirable
fibrosis. In this review, the role of
cytokines in wound healing and
fibrosis will be summarized and highlighted with more detailed discussion reserved for the possible points of therapeutic attack in
pulmonary fibrosis. In this review, the major
cytokines that are in current clinical use will be also discussed. In addition, advances in the application of novel
cytokines and anti-
cytokines for accelerating wound healing and attenuating
fibrosis both at the experimental and the clinical trial levels will be discussed.