Macrophages in the Aging Liver and Age-Related Liver Disease
Open accessAbstract
The number of individuals aged 65 or older is projected to increase globally from 524 million in 2010 to nearly 1. 5 billion in 2050. Aged individuals are particularly at risk for developing chronic illness, while being less able to regenerate healthy tissue and tolerate whole organ transplantation procedures. In the liver, these age-related diseases include non-alcoholic fatty liver disease, alcoholic liver disease, hepatitis, fibrosis, and cirrhosis. Hepatic macrophages, a population comprised of both Kupffer cells and infiltrating monocyte derived macrophages, are implicated in several chronic liver diseases and also play important roles in the homeostatic functions of the liver. The effects of aging on hepatic macrophage population dynamics, polarization, and function are not well understood. Studies performed on macrophages derived from other aged sources, such as the bone marrow, peritoneal cavity, lungs, and brain, demonstrate general reductions in autophagy and phagocytosis, dysfunction in cytokine signaling, and altered morphology and distribution, likely mediated by epigenetic changes and mitochondrial defects, that may be applicable to hepatic macrophages. This review highlights recent findings in macrophage developmental biology and function, particularly in the liver, and discusses the role of macrophages in various age-related liver diseases. A better understanding of the biology of aging that influences hepatic macrophages and thus the progression of chronic liver disease will be crucial in order to develop new interventions and treatments for liver disease in aging populations.
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Pro-inflammatory Kupffer cell activation is thought to contribute to age-related liver disease and to infectious diseases such as hepatitis.
“Activation of Kupffer cells to a pro-inflammatory state is thought to be a driver not only of ageing-related liver disease, such as non-alcoholic liver disease, cirrhosis and fibrosis, but also in the pathogenesis of infectious diseases such as hepatitis54.”
From Senescent cells promote tissue NAD+ decline during ageing via the activation of CD38+ macrophages (2020) · cites this paper as [54]
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Senescent cells promote tissue NAD+ decline during ageing via the activation of CD38+ macrophages
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- Authors
- Stahl, E. C., Haschak, M. J., Popovic, B., & Brown, B. N.
- Affiliations
- University of Pittsburgh (US)
- Corresponding author
- Brown, Bryan N.
- Venue
- Frontiers in Immunology
- Publisher
- Frontiers Media SA
- Published
- 2018-11-30
- Volume
- 9
- Pages
- 2795-2795
- ISSN
- 1664-3224 (ISSN-L)
- PMC
- PMC6284020
- OpenAlex
- W2903340170
- Cited by
- 171
- References
- 160
- Citations by year
- 2026: 13 · 2025: 17 · 2024: 25 · 2023: 43 · 2022: 16 · 2021: 33 · 2020: 16 · 2019: 7
- FWCI
- 1.89
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Frontiers in Immunology (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- National Institutes of Health
- National Institute on Aging (R01AG055564)
- National Institute of Diabetes and Digestive and Kidney Diseases (F31DK112633)
- National Institute of Biomedical Imaging and Bioengineering (T32EB001026)
- Topics
- Health Sciences › Medicine › Hepatology › Liver physiology and pathology
- Life Sciences › Immunology and Microbiology › Immunology › Immune cells in cancer
- Health Sciences › Medicine › Epidemiology › Liver Disease Diagnosis and Treatment
- Keywords
- hepatic macrophages, Kupffer cells, monocyte-derived macrophages, macrophage polarization, non-alcoholic fatty liver disease, alcoholic liver disease, liver fibrosis, liver cirrhosis, autophagy, phagocytosis, epigenetic modifications, mitochondrial dysfunction, chronic liver disease
- MeSH terms
- Aging, Animals, Autophagy, Humans, Kupffer Cells, Liver Diseases, Phagocytosis, Signal Transduction, Cytokines
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
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