Macrophages in age-related chronic inflammatory diseases
Open accessAbstract
Chronic inflammation is the common pathological basis for such age-associated diseases as cardiovascular disease, diabetes, cancer and Alzheimer’s disease. A multitude of bodily changes occur with aging that contribute to the initiation and development of inflammation. In particular, the immune system of elderly individuals often exhibits diminished efficiency and fidelity, termed immunosenescence. But, although immune responses to new pathogens and vaccines are impaired, immunosenescence is also characterized by a basal systemic inflammatory state. This alteration in immune system function likely promotes chronic inflammation. Changes in the tissue microenvironment, such as the accumulation of cell debris, and systemic changes in metabolic and hormonal signals, also likely contribute to the development of chronic inflammation. Monocyte/macrophage lineage cells are crucial to these age-associated changes, which culminate in the development of chronic inflammatory diseases. In this review, we will summarize the diverse physiological and pathological roles of macrophages in the chronic inflammation underlying age-associated diseases.
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Ageing leads to increased macrophage abundance and is accompanied by altered macrophage polarization state and function, which is emerging as a key driver of inflammageing.
“Although this observation was initially disregarded, there is now growing evidence that ageing not only leads to increased macrophage abundance but is also accompanied by altered macrophage polarization state and function, which is emerging as a key driver of inflammageing98,99.”
From NAD+ metabolism and its roles in cellular processes during ageing (2021) · cites this paper as [98]
Macrophages cause age-associated chronic inflammation.
“In addition to senescent cells, macrophages are also reported to cause age-associated chronic inflammation.44,45”
From Elimination of senescent cells by β-galactosidase-targeted prodrug attenuates inflammation and restores physical function in aged mice (2020) · cites this paper as [45]
SA-β-gal-positive macrophages can be harmful and accumulate in injured and aged tissues contributing to chronic inflammation.
“These SA-β-gal-positive macrophages can be harmful and have been found to accumulate in injured and aged tissues contributing to chronic inflammation.44,45”
From Elimination of senescent cells by β-galactosidase-targeted prodrug attenuates inflammation and restores physical function in aged mice (2020) · cites this paper as [45]
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- Authors
- Oishi, Y., & Manabe, I.
- Affiliations
- Tokyo Medical and Dental University (JP)
- Chiba University (JP)
- Corresponding author
- Oishi, Yumiko
- Manabe, Ichiro
- Venue
- npj Aging and Mechanisms of Disease
- Published
- 2016-07-28
- Volume
- 2
- Issue
- 1
- Pages
- 16018-16018
- ISSN
- 2056-3973 (ISSN-L)
- PMC
- PMC5515003
- OpenAlex
- W2489622437
- Cited by
- 262
- References
- 114
- Citations by year
- 2026: 16 · 2025: 31 · 2024: 30 · 2023: 28 · 2022: 29 · 2021: 25 · 2020: 44 · 2019: 21 · 2018: 21 · 2017: 14 · 2016: 1
- FWCI
- 1.83
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- npj Aging and Mechanisms of Disease (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Funders
- Japan Agency for Medical Research and Development (CREST)
- Ministry of Education, Culture, Sports, Science and Technology (16H05295, CREST)
- Japan Society for the Promotion of Science (25H10, 15H01506, CREST, 26461142, 16H05295)
- Core Research for Evolutional Science and Technology
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Immune cells in cancer
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Immunology and Microbiology › Immunology › Atherosclerosis and Cardiovascular Diseases
- Keywords
- macrophages, chronic inflammation, aging, immunosenescence, age-related diseases, cardiovascular disease, diabetes mellitus, cancer, Alzheimer's disease, monocyte/macrophage lineage, tissue microenvironment, cell debris
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