PerspectiveCell Biology

Cellular networks in wound healing

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Science  23 Nov 2018:
Vol. 362, Issue 6417, pp. 891-892
DOI: 10.1126/science.aav5542

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Summary

Restoration of tissue integrity and homeostasis after injury is fundamental to most organisms. Throughout evolution, there is diversity in whether the healing response replaces the damaged tissue through regeneration or by depositing collagenous connective tissue, defined as fibrosis. The molecular basis that underlies the repair response is complex. The postnatal decline of regenerative capacity in mammals as well as the regenerative heterogeneity among diverse organs is an unresolved obstacle in medicine. Limited fibrosis to temporarily stabilize newly forming tissue is important for healing but ultimately impairs tissue function. Disorders characterized by excessive fibrosis—including interstitial lung disease; fibrosis of the liver or kidney; sclerosing skin diseases; and localized fibrotic manifestations associated with, for example, late stage venous insufficiency, skin fragility disorders, trauma, or cancer—contribute considerably to patient discomfort and morbidity as well as high numbers of deaths worldwide. Nonetheless, progression in the development of antifibrotic therapeutics is slow (1). On page 909 of this issue, Shook et al. (2) identify a critical role of fibroblast and immune cell heterogeneity and communication in promoting efficient skin wound healing. These findings add to the understanding of fibrosis and could guide us toward better treatments for fibrosing diseases.

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