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Trends Immunol. 2019 Feb;40(2):113-127. doi: 10.1016/j.it.2018.12.007. Epub 2019 Jan 6.

Metabolic Alterations in Aging Macrophages: Ingredients for Inflammaging?

Author information

1
Top Institute Food and Nutrition, Nieuwe Kanaal 9A, 6709 PA Wageningen, The Netherlands; Cell Biology and Immunology Group, Wageningen University, De Elst 1, 6709 PG Wageningen, The Netherlands; Department of Immunology, Erasmus University Medical Center, Wytemaweg 80, 3015 CN Rotterdam, The Netherlands.
2
Amsterdam UMC, Vrije Universiteit Amsterdam, Department of Molecular Cell Biology and Immunology, Amsterdam Cardiovascular Sciences, Cancer Center Amsterdam, De Boelelaan 1117, Amsterdam, Netherlands; Amsterdam UMC, University of Amsterdam, Experimental Vascular Biology, Department of Medical Biochemistry, Amsterdam Cardiovascular Sciences, Meibergdreef 9, Amsterdam, The Netherlands.
3
Department of Genetics, Erasmus University Medical Center, Wytemaweg 80, 3015 CN Rotterdam, The Netherlands.
4
Amsterdam UMC, University of Amsterdam, Experimental Vascular Biology, Department of Medical Biochemistry, Amsterdam Cardiovascular Sciences, Meibergdreef 9, Amsterdam, The Netherlands; Institute for Cardiovascular Prevention (IPEK), Munich, Germany.
5
Department of Immunology, Erasmus University Medical Center, Wytemaweg 80, 3015 CN Rotterdam, The Netherlands. Electronic address: p.leenen@erasmusmc.nl.

Abstract

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.

KEYWORDS:

aging; cell metabolism; epigenetics; inflammation; macrophages

PMID:
30626541
DOI:
10.1016/j.it.2018.12.007

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