Metabolic Alterations in Aging Macrophages: Ingredients for Inflammaging?

Adriaan A. van Beek, Jan van den Bossche, Pier G. Mastroberardino, Menno P. J. de Winther, Pieter J. M. Leenen

Research output: Contribution to journalReview articleAcademicpeer-review

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.
Original languageEnglish
Pages (from-to)113-127
JournalTrends in Immunology
Volume40
Issue number2
DOIs
Publication statusPublished - 2019

Cite this

van Beek, A. A., van den Bossche, J., Mastroberardino, P. G., de Winther, M. P. J., & Leenen, P. J. M. (2019). Metabolic Alterations in Aging Macrophages: Ingredients for Inflammaging? Trends in Immunology, 40(2), 113-127. https://doi.org/10.1016/j.it.2018.12.007
van Beek, Adriaan A. ; van den Bossche, Jan ; Mastroberardino, Pier G. ; de Winther, Menno P. J. ; Leenen, Pieter J. M. / Metabolic Alterations in Aging Macrophages: Ingredients for Inflammaging?. In: Trends in Immunology. 2019 ; Vol. 40, No. 2. pp. 113-127.
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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.",
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van Beek, AA, van den Bossche, J, Mastroberardino, PG, de Winther, MPJ & Leenen, PJM 2019, 'Metabolic Alterations in Aging Macrophages: Ingredients for Inflammaging?' Trends in Immunology, vol. 40, no. 2, pp. 113-127. https://doi.org/10.1016/j.it.2018.12.007

Metabolic Alterations in Aging Macrophages: Ingredients for Inflammaging? / van Beek, Adriaan A.; van den Bossche, Jan; Mastroberardino, Pier G.; de Winther, Menno P. J.; Leenen, Pieter J. M.

In: Trends in Immunology, Vol. 40, No. 2, 2019, p. 113-127.

Research output: Contribution to journalReview articleAcademicpeer-review

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AB - 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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