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肾损伤与修复中的巨噬细胞多样性

Macrophage diversity in renal injury and repair.

作者信息

Ricardo Sharon D, van Goor Harry, Eddy Allison A

机构信息

Monash Immunology and Stem Cell Laboratories, Monash University, Clayton, Victoria, Australia.

出版信息

J Clin Invest. 2008 Nov;118(11):3522-30. doi: 10.1172/JCI36150.

DOI:10.1172/JCI36150
PMID:18982158
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2575702/
Abstract

Monocyte-derived macrophages can determine the outcome of the immune response and whether this response contributes to tissue repair or mediates tissue destruction. In addition to their important role in immune-mediated renal disease and host defense, macrophages play a fundamental role in tissue remodeling during embryonic development, acquired kidney disease, and renal allograft responses. This review summarizes macrophage phenotype and function in the orchestration of kidney repair and replacement of specialized renal cells following injury. Recent advances in our understanding of macrophage heterogeneity in response to their microenvironment raise new and exciting therapeutic possibilities to attenuate or conceivably reverse progressive renal disease in the context of fibrosis. Furthermore, parallels with pathological processes in many other organs also exist.

摘要

单核细胞衍生的巨噬细胞能够决定免疫反应的结果,以及这种反应是有助于组织修复还是介导组织破坏。除了在免疫介导的肾脏疾病和宿主防御中发挥重要作用外,巨噬细胞在胚胎发育、后天性肾脏疾病和肾移植反应期间的组织重塑中也发挥着重要作用。本综述总结了巨噬细胞在肾脏损伤修复和损伤后特殊肾细胞替代过程中的表型和功能。我们对巨噬细胞在响应其微环境时的异质性的最新认识进展,为在纤维化背景下减轻或可能逆转进行性肾脏疾病带来了新的、令人兴奋的治疗可能性。此外,与许多其他器官的病理过程也存在相似之处。

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本文引用的文献

1
Pathogen destruction versus intracellular survival: the role of lipids as phagosomal fate determinants.病原体破坏与细胞内存活:脂质作为吞噬体命运决定因素的作用
J Clin Invest. 2008 Jun;118(6):2002-11. doi: 10.1172/JCI35433.
2
IKKbeta/NF-kappaB and the miscreant macrophage.IKKβ/NF-κB与不良巨噬细胞
J Exp Med. 2008 Jun 9;205(6):1255-9. doi: 10.1084/jem.20081056. Epub 2008 Jun 2.
3
Production of type VI collagen by human macrophages: a new dimension in macrophage functional heterogeneity.人类巨噬细胞产生VI型胶原蛋白:巨噬细胞功能异质性的新维度。
J Immunol. 2008 Apr 15;180(8):5707-19. doi: 10.4049/jimmunol.180.8.5707.
4
Systemic gene therapy with interleukin-13 attenuates renal ischemia-reperfusion injury.白细胞介素-13全身基因治疗可减轻肾脏缺血再灌注损伤。
Kidney Int. 2008 Jun;73(12):1364-73. doi: 10.1038/ki.2008.18. Epub 2008 Mar 19.
5
Remodeling phenotype of human subcutaneous adipose tissue macrophages.人类皮下脂肪组织巨噬细胞的重塑表型
Circulation. 2008 Feb 12;117(6):806-15. doi: 10.1161/CIRCULATIONAHA.107.724096. Epub 2008 Jan 28.
6
IL-22 is required for Th17 cell-mediated pathology in a mouse model of psoriasis-like skin inflammation.在银屑病样皮肤炎症小鼠模型中,白细胞介素-22是辅助性T细胞17(Th17)细胞介导的病理过程所必需的。
J Clin Invest. 2008 Feb;118(2):597-607. doi: 10.1172/JCI33263.
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Hepatocyte growth factor suppresses proinflammatory NFkappaB activation through GSK3beta inactivation in renal tubular epithelial cells.肝细胞生长因子通过使肾小管上皮细胞中的糖原合成酶激酶3β失活来抑制促炎性核因子κB的激活。
J Biol Chem. 2008 Mar 21;283(12):7401-10. doi: 10.1074/jbc.M710396200. Epub 2008 Jan 17.
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Molecular mechanisms linking wound inflammation and fibrosis: knockdown of osteopontin leads to rapid repair and reduced scarring.连接伤口炎症和纤维化的分子机制:骨桥蛋白的敲低导致快速修复并减少疤痕形成。
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Chemokine receptor CX3CR1 mediates skin wound healing by promoting macrophage and fibroblast accumulation and function.趋化因子受体CX3CR1通过促进巨噬细胞和成纤维细胞的聚集及功能来介导皮肤伤口愈合。
J Immunol. 2008 Jan 1;180(1):569-79. doi: 10.4049/jimmunol.180.1.569.
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The healing myocardium sequentially mobilizes two monocyte subsets with divergent and complementary functions.正在愈合的心肌会依次动员两个具有不同且互补功能的单核细胞亚群。
J Exp Med. 2007 Nov 26;204(12):3037-47. doi: 10.1084/jem.20070885. Epub 2007 Nov 19.