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慢性难愈合糖尿病伤口中细胞凋亡相关性的最新进展

Recent advances on the association of apoptosis in chronic non healing diabetic wound.

作者信息

Arya Awadhesh K, Tripathi Richik, Kumar Santosh, Tripathi Kamlakar

机构信息

Awadhesh K Arya, Faculty of Health Sciences, Department of Microbiology, Immunology and Genetics, Ben Gurion University of The Negev, Beer Sheva 8410501, Israel.

出版信息

World J Diabetes. 2014 Dec 15;5(6):756-62. doi: 10.4239/wjd.v5.i6.756.

DOI:10.4239/wjd.v5.i6.756
PMID:25512778
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4265862/
Abstract

Generally, wounds are of two categories, such as chronic and acute. Chronic wounds takes time to heal when compared to the acute wounds. Chronic wounds include vasculitis, non healing ulcer, pyoderma gangrenosum, and diseases that cause ischemia. Chronic wounds are rapidly increasing among the elderly population with dysfunctional valves in their lower extremity deep veins, ulcer, neuropathic foot and pressure ulcers. The process of the healing of wounds has several steps with the involvement of immune cells and several other cell types. There are many evidences supporting the hypothesis that apoptosis of immune cells is involved in the wound healing process by ending inflammatory condition. It is also involved in the resolution of various phases of tissue repair. During final steps of wound healing most of the endothelial cells, macrophages and myofibroblasts undergo apoptosis or exit from the wound, leaving a mass that contains few cells and consists mostly of collagen and other extracellular matrix proteins to provide strength to the healing tissue. This review discusses the various phases of wound healing both in the chronic and acute wounds especially during diabetes mellitus and thus support the hypothesis that the oxidative stress, apoptosis, connexins and other molecules involved in the regulation of chronic wound healing in diabetes mellitus and gives proper understanding of the mechanisms controlling apoptosis and tissue repair during diabetes and may eventually develop therapeutic modalities to fasten the healing process in diabetic patients.

摘要

一般来说,伤口分为两类,即慢性伤口和急性伤口。与急性伤口相比,慢性伤口愈合需要时间。慢性伤口包括血管炎、不愈合溃疡、坏疽性脓皮病以及导致局部缺血的疾病。在下肢深静脉瓣膜功能不全、溃疡、神经性足病和压疮的老年人群中,慢性伤口正在迅速增加。伤口愈合过程有几个步骤,涉及免疫细胞和其他几种细胞类型。有许多证据支持这样的假说,即免疫细胞的凋亡通过结束炎症状态参与伤口愈合过程。它还参与组织修复各个阶段的消退。在伤口愈合的最后阶段,大多数内皮细胞、巨噬细胞和成肌纤维细胞会发生凋亡或离开伤口,留下一个细胞很少、主要由胶原蛋白和其他细胞外基质蛋白组成的团块,为愈合组织提供强度。本综述讨论了慢性和急性伤口愈合的各个阶段,特别是在糖尿病期间的情况,从而支持了氧化应激、凋亡、连接蛋白和其他参与糖尿病慢性伤口愈合调节的分子的假说,并对糖尿病期间控制凋亡和组织修复的机制有了恰当的理解,最终可能开发出治疗方法来加速糖尿病患者的愈合过程。

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本文引用的文献

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Differential Apoptosis in Mucosal and Dermal Wound Healing.黏膜和皮肤伤口愈合中的差异性细胞凋亡
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Neutrophils and natural killer T cells as negative regulators of wound healing.中性粒细胞和自然杀伤T细胞作为伤口愈合的负调节因子。
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Apoptotic cells activate the "phoenix rising" pathway to promote wound healing and tissue regeneration.凋亡细胞激活“凤凰涅槃”通路,促进伤口愈合和组织再生。
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