伤口愈合
血管生成
医学
基质金属蛋白酶
糖尿病
角质形成细胞
炎症
下调和上调
免疫学
癌症研究
内分泌学
内科学
生物
细胞培养
遗传学
基因
生物化学
作者
Stephen Chu‐Sung Hu,Cheng‐Che E. Lan
标识
DOI:10.1016/j.jdermsci.2016.07.008
摘要
Impaired wound healing is a common and potentially serious complication in patients with diabetes. In recent years, disturbed physiologic functions of epidermal keratinocytes have been found to play a central role in the poor healing ability of diabetic wounds. Factors involving keratinocytes that may contribute to the dysfunctional wound healing process in diabetes include impaired keratinocyte migration and proliferation, gap junction abnormalities, chronic inflammation, chronic infections associated with defective innate immunity, impaired angiogenesis, increased oxidative stress, and abnormal expression of matrix metalloproteinases (MMPs). In this review article, we provide evidence from the scientific literature for the molecular mechanisms of delayed wound healing in diabetes, with particular emphasis on keratinocytes. Elucidating the spectrum of molecular and functional abnormalities in keratinocytes induced by high-glucose environment may lead to more effective and individualized therapeutic strategies for the prevention and management of chronic diabetic wounds.
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