Macrophages in Tissue Repair, Regeneration, and Fibrosis.
Macrophages in Tissue Repair, Regeneration, and Fibrosis.
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巨噬细胞与组织修复、再生和纤维化。
DOI：
10.1016/j.immuni.2016.02.015
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发表时间：
2016-03-15
期刊：
影响因子：
32.4
通讯作者：
Vannella KM
中科院分区：
文献类型：
--
作者：
Wynn TA;Vannella KM
炎性单核细胞和常驻组织巨噬细胞是组织修复、再生和纤维化的关键调节细胞。在组织损伤后，单核细胞和巨噬细胞经历了显著的表型和功能变化，在组织修复的启动、维持和解决阶段发挥了关键作用。巨噬细胞功能紊乱可导致异常修复，炎症介质和生长因子的产生失控，抗炎巨噬细胞生成不足，巨噬细胞与上皮细胞、内皮细胞、成纤维细胞、干细胞或组织前体细胞之间的通讯障碍，这些都可能导致持续性损伤状态，从而导致病理性纤维化的发展。在这篇综述中，我们讨论了引导巨噬细胞在损伤后采取促炎、促伤口愈合、促纤维化、抗炎、抗纤维化、促分解和组织再生表型的机制，并强调了其中一些机制和巨噬细胞激活状态如何被用于治疗。
Inflammatory monocytes and resident tissue macrophages are key regulators of tissue repair, regeneration, and fibrosis. Following tissue injury, monocytes and macrophages undergo marked phenotypic and functional changes to play critical roles during the initiation, maintenance, and resolution phases of tissue repair. Disturbances in macrophage function can lead to aberrant repair, with uncontrolled inflammatory mediator and growth factor production, deficient generation of anti-inflammatory macrophages, or failed communication between macrophages and epithelial cells, endothelial cells, fibroblasts, and stem or tissue progenitor cells all contributing to a state of persistent injury, which may lead to the development of pathological fibrosis. In this review, we discuss the mechanisms that instruct macrophages to adopt pro-inflammatory, pro-wound healing, pro-fibrotic, anti-inflammatory, anti-fibrotic, pro-resolving, and tissue regenerating phenotypes following injury, and highlight how some of these mechanisms and macrophage activation states could be exploited therapeutically.