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Cell Mol Life Sci. 2016 Oct;73(20):3861-85. doi: 10.1007/s00018-016-2268-0. Epub 2016 May 14.

Transition from inflammation to proliferation: a critical step during wound healing.

Author information

1
Unit of Dermatology and Venereology, Molecular Dermatology Research Group, Department of Medicine, Center for Molecular Medicine (CMM), L8:02, Karolinska Institutet, SE-171 76, Stockholm, Sweden. ning.xu@ki.se.
2
Unit of Dermatology and Venereology, Karolinska University Hospital, Solna, Sweden. ning.xu@ki.se.
3
Unit of Dermatology and Venereology, Molecular Dermatology Research Group, Department of Medicine, Center for Molecular Medicine (CMM), L8:02, Karolinska Institutet, SE-171 76, Stockholm, Sweden.
4
Unit of Dermatology and Venereology, Karolinska University Hospital, Solna, Sweden.

Abstract

The ability to rapidly restore the integrity of a broken skin barrier is critical and is the ultimate goal of therapies for hard-to-heal-ulcers. Unfortunately effective treatments to enhance healing and reduce scarring are still lacking. A deeper understanding of the physiology of normal repair and of the pathology of delayed healing is a prerequisite for the development of more effective therapeutic interventions. Transition from the inflammatory to the proliferative phase is a key step during healing and accumulating evidence associates a compromised transition with wound healing disorders. Thus, targeting factors that impact this phase transition may offer a rationale for therapeutic development. This review summarizes mechanisms regulating the inflammation-proliferation transition at cellular and molecular levels. We propose that identification of such mechanisms will reveal promising targets for development of more effective therapies.

KEYWORDS:

Bioactive lipid mediator; Fibroblast; Macrophage; MicroRNA; Reactive oxygen species; Toll-like receptor; Transcription factor

PMID:
27180275
PMCID:
PMC5021733
DOI:
10.1007/s00018-016-2268-0
[Indexed for MEDLINE]
Free PMC Article

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