期刊
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
卷 21, 期 3, 页码 -出版社
MDPI
DOI: 10.3390/ijms21031105
关键词
fibrosis; wound healing; burn; hypertrophic scarring; myofibroblasts; macrophages; inflammation; EMT
资金
- National Institute of General Medical Sciences of the National Institutes of Health [T32GM008256]
Cutaneous fibrosis results from suboptimal wound healing following significant tissue injury such as severe burns, trauma, and major surgeries. Pathologic skin fibrosis results in scars that are disfiguring, limit normal movement, and prevent patient recovery and reintegration into society. While various therapeutic strategies have been used to accelerate wound healing and decrease the incidence of scarring, recent studies have targeted the molecular regulators of each phase of wound healing, including the inflammatory, proliferative, and remodeling phases. Here, we reviewed the most recent literature elucidating molecular pathways that can be targeted to reduce fibrosis with a particular focus on post-burn scarring. Current research targeting inflammatory mediators, the epithelial to mesenchymal transition, and regulators of myofibroblast differentiation shows promising results. However, a multimodal approach addressing all three phases of wound healing may provide the best therapeutic outcome.
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