Macrophages in inflammation, repair and regeneration
Macrophages in inflammation, repair and regeneration
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DOI：
10.1093/intimm/dxy054
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发表时间：
2018-11-01
影响因子：
4.4
通讯作者：
Manabe, Ichiro
中科院分区：
文献类型：
--
作者：
Oishi, Yumiko;Manabe, Ichiro
组织损伤触发一系列复杂的细胞反应，从组织和细胞损伤激活的炎症开始，并继续愈合。通过清除细胞碎片，激活和解决炎症和促进纤维化，巨噬细胞在大多数（如果不是所有）损伤反应阶段中发挥关键作用。最近对最初炎症和后来组织再生和修复的机制的研究表明，巨噬细胞部分通过支持和激活干/祖细胞、清除受损组织、重塑细胞外基质以准备再生支架和促进血管生成来桥接这些过程。然而，巨噬细胞在由消退失败（例如慢性炎症）和过度瘢痕形成诱导的病理学发展中也具有中心作用。在这篇综述中，我们总结了巨噬细胞在炎症和愈合中的活动，以应对不同再生能力的组织中的急性损伤。虽然巨噬细胞在这些组织中对组织损伤的反应中导致类似的过程，但它们的优先级和它们的活动的后果在组织中不同。此外，损伤的程度、性质和持续时间也极大地影响细胞反应和愈合过程。特别是，持续的损伤和/或炎症的消退失败导致慢性疾病，其中巨噬细胞活性可能变得有害。
Tissue injury triggers a complex series of cellular responses, starting from inflammation activated by tissue and cell damage and proceeding to healing. By clearing cell debris, activating and resolving inflammation and promoting fibrosis, macrophages play key roles in most, if not all, phases of the response to injury. Recent studies of the mechanisms underlying the initial inflammation and later tissue regeneration and repair revealed that macrophages bridge these processes in part by supporting and activating stem/progenitor cells, clearing damaged tissue, remodeling extracellular matrix to prepare scaffolding for regeneration and promoting angiogenesis. However, macrophages also have a central role in the development of pathology induced by failed resolution (e.g. chronic inflammation) and excessive scarring. In this review, we summarize the activities of macrophages in inflammation and healing in response to acute injury in tissues with differing regenerative capacities. While macrophages lead similar processes in response to tissue injury in these tissues, their priorities and the consequences of their activities differ among tissues. Moreover, the magnitude, nature and duration of injury also greatly affect cellular responses and healing processes. In particular, continuous injury and/or failed resolution of inflammation leads to chronic ailments in which macrophage activities may become detrimental.