Macrophage Phenotypes Regulate Scar Formation and Chronic Wound Healing.
| Autor: | Hesketh M; The Institute for Health and Biomedical Innovation, School of Biomedical Sciences, Faculty of Health, Queensland University of Technology, Brisbane QLD 4059, Australia. m.hesketh@connect.qut.edu.au., Sahin KB; The Institute for Health and Biomedical Innovation, School of Biomedical Sciences, Faculty of Health, Queensland University of Technology, Brisbane QLD 4059, Australia. katherine.sahin@connect.qut.edu.au., West ZE; The Institute for Health and Biomedical Innovation, School of Biomedical Sciences, Faculty of Health, Queensland University of Technology, Brisbane QLD 4059, Australia. zoe.west@connect.qut.edu.au., Murray RZ; The Institute for Health and Biomedical Innovation, School of Biomedical Sciences, Faculty of Health, Queensland University of Technology, Brisbane QLD 4059, Australia. rachael.murray@qut.edu.au. |
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| Jazyk: | angličtina |
| Zdroj: | International journal of molecular sciences [Int J Mol Sci] 2017 Jul 17; Vol. 18 (7). Date of Electronic Publication: 2017 Jul 17. |
| DOI: | 10.3390/ijms18071545 |
| Abstrakt: | 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. Competing Interests: The authors declare no conflict of interest. |
| Databáze: | MEDLINE |
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