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Title: | Macrophages: versatile players in renal inflammation and fibrosis. | Authors: | Lan H.-Y.;Tang P.M.-K.;Nikolic-Paterson D.J. | Institution: | (Tang, Lan) Department of Medicine & Therapeutics, Li Ka Shing Institute of Health Sciences, and Lui Che Woo Institute of Innovative Medicine, The Chinese University of Hong Kong, Shatin, Hong Kong (Tang) Department of Anatomical and Cellular Pathology, State Key Laboratory of Translational Oncology, Prince of Wales Hospital, The Chinese University of Hong Kong, Shatin, Hong Kong (Nikolic-Paterson) Department of Nephrology, Monash Medical Centre and Monash University Centre for Inflammatory Diseases, Melbourne, VIC, Australia | Issue Date: | 1-Mar-2019 | Copyright year: | 2019 | Publisher: | Nature Publishing Group (Houndmills, Basingstoke, Hampshire RG21 6XS, United Kingdom) | Place of publication: | United Kingdom | Publication information: | Nature Reviews Nephrology. 15 (3) (pp 144-158), 2019. Date of Publication: 01 Mar 2019. | Journal: | Nature Reviews Nephrology | Abstract: | Macrophages have important roles in immune surveillance and in the maintenance of kidney homeostasis; their response to renal injury varies enormously depending on the nature and duration of the insult. Macrophages can adopt a variety of phenotypes: at one extreme, M1 pro-inflammatory cells contribute to infection clearance but can also promote renal injury; at the other extreme, M2 anti-inflammatory cells have a reparative phenotype and can contribute to the resolution phase of the response to injury. In addition, bone marrow monocytes can differentiate into myeloid-derived suppressor cells that can regulate T cell immunity in the kidney. However, macrophages can also promote renal fibrosis, a major driver of progression to end-stage renal disease, and the CD206+ subset of M2 macrophages is strongly associated with renal fibrosis in both human and experimental diseases. Myofibroblasts are important contributors to renal fibrosis and recent studies provide evidence that macrophages recruited from the bone marrow can transition directly into myofibroblasts within the injured kidney. This process is termed macrophage-to-myofibroblast transition (MMT) and is driven by transforming growth factor-beta1 (TGFbeta1)-Smad3 signalling via a Src-centric regulatory network. MMT may serve as a key checkpoint for the progression of chronic inflammation into pathogenic fibrosis.Copyright © 2019, Springer Nature Limited. | DOI: | http://monash.idm.oclc.org/login?url=http://dx.doi.org/10.1038/s41581-019-0110-2 | PubMed URL: | 30692665 [http://www.ncbi.nlm.nih.gov/pubmed/?term=30692665] | ISSN: | 1759-5061 | URI: | https://repository.monashhealth.org/monashhealthjspui/handle/1/35828 | Type: | Review | Subjects: | cell proliferation chronic inflammation disease association human *kidney fibrosis kidney injury *macrophage monocyte myofibroblast *nephritis nonhuman priority journal review signal transduction Smad3 protein/ec [Endogenous Compound] transforming growth factor beta1/ec [Endogenous Compound] myeloid-derived suppressor cell acute kidney failure cell heterogeneity cell plasticity myeloid-derived suppressor cell myofibroblast *nephritis nonhuman priority journal Review signal transduction human disease association chronic inflammation cell proliferation *kidney fibrosis cell heterogeneity acute kidney failure kidney injury monocyte cell plasticity *macrophage |
Type of Clinical Study or Trial: | Review article (e.g. literature review, narrative review) |
Appears in Collections: | Articles |
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