医学
伤口愈合
血管生成
人口
成纤维细胞
重症监护医学
生物信息学
免疫学
癌症研究
生物
生物化学
环境卫生
体外
作者
Helen A. Thomason,Matthew J. Hardman
标识
DOI:10.1017/s095925980999027x
摘要
Summary Our ability to heal wounds deteriorates with age, leading in many cases to a complete lack of repair and development of a chronic wound. Moreover, as the elderly population continues to grow the prevalence of non-healing chronic wounds is escalating. Cutaneous wound repair occurs through a combination of overlapping phases, including an initial inflammatory response, a proliferative phase and a final remodelling phase. In elderly subjects the inflammatory response is delayed, macrophage and fibroblast function compromised, angiogenesis reduced and re-epithelialization inhibited. Whilst a large body of historic research describes the defective processes that lead to delayed healing, only recently have the molecular mechanisms by which these defects arise begun to be elucidated. Current therapies available for treatment of chronic wounds in elderly people are surprisingly limited and generally ineffective. Thus there is an urgent need to develop new therapeutic strategies based on these recent molecular and cellular insights.
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