炎症
细胞因子
内质网
表型
细胞生物学
生物
巨噬细胞
衰老
线粒体
平衡
免疫学
体外
生物化学
基因
作者
Adriaan A. van Beek,Jan Van den Bossche,Pier G. Mastroberardino,Menno P.J. de Winther,Pieter J. M. Leenen
标识
DOI:10.1016/j.it.2018.12.007
摘要
Aging is a complex process with an impact on essentially all organs. Declined cellular repair causes increased damage at genomic and proteomic levels upon aging. This can lead to systemic changes in metabolism and pro-inflammatory cytokine production, resulting in low-grade inflammation, or 'inflammaging'. Tissue macrophages, gatekeepers of parenchymal homeostasis and integrity, are prime inflammatory cytokine producers, as well as initiators and regulators of inflammation. In this opinion piece, we summarize intrinsic alterations in macrophage phenotype and function with age. We propose that alternatively activated macrophages (M2-like), which are yet pro-inflammatory, can accumulate in tissues and promote inflammaging. Age-related increases in endoplasmic reticulum stress and mitochondrial dysfunction might be cell-intrinsic forces driving this unusual phenotype.
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