Journal
CELLULAR AND MOLECULAR LIFE SCIENCES
Volume 73, Issue 20, Pages 3861-3885Publisher
SPRINGER BASEL AG
DOI: 10.1007/s00018-016-2268-0
Keywords
Macrophage; Fibroblast; Bioactive lipid mediator; Reactive oxygen species; Toll-like receptor; Transcription factor; MicroRNA
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Funding
- Swedish Research Council [K2014-85X-22500-01-3]
- Ragnar Soderbergs Foundation
- Hedlunds Foundation
- Welander and Finsens Foundation
- Ake Wibergs Foundation
- Jeanssons Foundation
- Karolinska Institutet
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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.
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