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Advances in the modulation of cutaneous wound healing and scarring.

机译:调节皮肤伤口愈合和瘢痕形成的研究进展。

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摘要

Cutaneous wounds inevitably heal with scars, which can be disfiguring and compromise function. In general, the greater the insult, the worse the scarring, although genetic make up, regional variations and age can influence the final result. Excessive scarring manifests as hypertrophic and keloid scars. At the other end of the spectrum are poorly healing chronic wounds, such as foot ulcers in diabetic patients and pressure sores. Current therapies to minimize scarring and accelerate wound healing rely on the optimization of systemic conditions, early wound coverage and closure of lacerations, and surgical incisions with minimal trauma to the surrounding skin. The possible benefits of topical therapies have also been assessed. Further major improvements in wound healing and scarring require an understanding of the molecular basis of this process. Promising strategies for modulating healing include the local administration of platelet derived growth factor (PDGF)-BB to accelerate the healing of chronic ulcers, and increasing the relative ratio of transforming growth factor (TGF)beta-3 to TGFbeta-1 and TGFbeta-2 in order to minimize scarring.
机译:皮肤伤口不可避免地会愈合,并会留下疤痕,这可能会毁容并损害功能。通常,侮辱越大,疤痕越糟,尽管遗传组成,区域差异和年龄会影响最终结果。过多的疤痕表现为肥大性瘢痕和瘢痕loid。另一方面,慢性伤口愈合不良,例如糖尿病患者的足部溃疡和褥疮。当前使疤痕最小化并加速伤口愈合的疗法依赖于全身状况的优化,伤口的早期覆盖和撕裂的闭合以及对周围皮肤的创伤最小的手术切口。还评估了局部疗法的可能益处。伤口愈合和瘢痕形成的进一步重大改进需要了解该过程的分子基础。调节愈合的有希望的策略包括局部施用血小板衍生生长因子(PDGF)-BB来加速慢性溃疡的愈合,并增加转化生长因子(TGF)beta-3与TGFbeta-1和TGFbeta-2的相对比例为了减少疤痕。

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