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

被引:1246
作者
Landen, Ning Xu [1 ,2 ]
Li, Dongqing [1 ,2 ]
Stahle, Mona [1 ,2 ]
机构
[1] Karolinska Inst, Ctr Mol Med CMM, Mol Dermatol Res Grp, Unit Dermatol & Venereol,Dept Med, L8 02, SE-17176 Stockholm, Sweden
[2] Karolinska Univ Hosp, Unit Dermatol & Venereol, Solna, Sweden
基金
瑞典研究理事会;
关键词
Macrophage; Fibroblast; Bioactive lipid mediator; Reactive oxygen species; Toll-like receptor; Transcription factor; MicroRNA; ENDOTHELIAL GROWTH-FACTOR; ALTERNATIVELY ACTIVATED MACROPHAGES; HISTONE DEACETYLASE INHIBITORS; TOLL-LIKE RECEPTORS; T-CELLS; MICE LACKING; HUMAN-SKIN; MATRIX METALLOPROTEINASES; TRANSCRIPTIONAL CONTROL; EPIGENETIC REGULATION;
D O I
10.1007/s00018-016-2268-0
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
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.
引用
收藏
页码:3861 / 3885
页数:25
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