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巨噬细胞表型调节瘢痕形成和慢性伤口愈合。

Macrophage Phenotypes Regulate Scar Formation and Chronic Wound Healing.

作者信息

Hesketh Mark, Sahin Katherine B, West Zoe E, Murray Rachael Z

机构信息

The Institute for Health and Biomedical Innovation, School of Biomedical Sciences, Faculty of Health, Queensland University of Technology, Brisbane QLD 4059, Australia.

出版信息

Int J Mol Sci. 2017 Jul 17;18(7):1545. doi: 10.3390/ijms18071545.

DOI:10.3390/ijms18071545
PMID:28714933
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5536033/
Abstract

Macrophages and inflammation play a beneficial role during wound repair with macrophages regulating a wide range of processes, such as removal of dead cells, debris and pathogens, through to extracellular matrix deposition re-vascularisation and wound re-epithelialisation. To perform this range of functions, these cells develop distinct phenotypes over the course of wound healing. They can present with a pro-inflammatory M1 phenotype, more often found in the early stages of repair, through to anti-inflammatory M2 phenotypes that are pro-repair in the latter stages of wound healing. There is a continuum of phenotypes between these ranges with some cells sharing phenotypes of both M1 and M2 macrophages. One of the less pleasant consequences of quick closure, namely the replacement with scar tissue, is also regulated by macrophages, through their promotion of fibroblast proliferation, myofibroblast differentiation and collagen deposition. Alterations in macrophage number and phenotype disrupt this process and can dictate the level of scar formation. It is also clear that dysregulated inflammation and altered macrophage phenotypes are responsible for hindering closure of chronic wounds. The review will discuss our current knowledge of macrophage phenotype on the repair process and how alterations in the phenotypes might alter wound closure and the final repair quality.

摘要

巨噬细胞和炎症在伤口修复过程中发挥着有益作用,巨噬细胞调节着广泛的过程,如清除死细胞、碎片和病原体,直至细胞外基质沉积、血管再形成和伤口再上皮化。为了执行这一系列功能,这些细胞在伤口愈合过程中会形成不同的表型。它们可以呈现促炎的M1表型,这种表型在修复早期更为常见,也可以呈现抗炎的M2表型,后者在伤口愈合后期具有促进修复的作用。在这些范围之间存在着一系列连续的表型,一些细胞同时具有M1和M2巨噬细胞的表型特征。快速愈合带来的一个不太令人满意的后果,即被瘢痕组织替代,也受到巨噬细胞的调控,巨噬细胞通过促进成纤维细胞增殖、肌成纤维细胞分化和胶原蛋白沉积来实现这一调控。巨噬细胞数量和表型的改变会破坏这一过程,并可能决定瘢痕形成的程度。同样明显的是,炎症失调和巨噬细胞表型改变是阻碍慢性伤口愈合的原因。本综述将讨论我们目前对巨噬细胞表型在修复过程中的认识,以及表型改变如何可能影响伤口愈合和最终的修复质量。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ba32/5536033/421b60709769/ijms-18-01545-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ba32/5536033/cd3feb9b2b13/ijms-18-01545-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ba32/5536033/421b60709769/ijms-18-01545-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ba32/5536033/cd3feb9b2b13/ijms-18-01545-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ba32/5536033/421b60709769/ijms-18-01545-g002.jpg

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