Inflammaging and ‘Garb-aging’
Open accessAbstract
'Inflammaging' refers to the chronic, low-grade inflammation that characterizes aging. Inflammaging is macrophage centered, involves several tissues and organs, including the gut microbiota, and is characterized by a complex balance between pro- and anti-inflammatory responses. Based on literature data, we argue that the major source of inflammatory stimuli is represented by endogenous/self, misplaced, or altered molecules resulting from damaged and/or dead cells and organelles (cell debris), recognized by receptors of the innate immune system. While their production is physiological and increases with age, their disposal by the proteasome via autophagy and/or mitophagy progressively declines. This 'autoreactive/autoimmune' process fuels the onset or progression of chronic diseases that can accelerate and propagate the aging process locally and systemically. Consequently, inflammaging can be considered a major target for antiaging strategies.
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The production of inflammatory cell death modalities and endogenous molecular garbage, such as mitochondrial RNA, misplaced molecules, and cell debris, is a causal inflammatory stimulus that can accelerate inflammaging.
“A newly developed conception, garb-aging, reveals that the production of inflammatory cell death modalities, endogenous molecular garbage (e.g., mitochondrial RNA, misplaced molecules, and cell debris), is a causal inflammatory stimuli that can accelerate inflammaging.227,228”
From Inflammation and aging: signaling pathways and intervention therapies (2023) · cites this paper as [227]
In “Where do the stimuli fuelling inflammaging come from?” (page unavailable), the authors argue that an age-related imbalance between the production and disposal of cell debris and misplaced self-molecules fuels inflammaging. The paper discusses mitochondrial DNA as an inflammatory stimulus, not mitochondrial RNA, and the passages do not identify inflammatory cell-death modalities as such a stimulus. (LLM, conf=0.87)
Experimental — accuracy not yet measuredThe local low-grade inflammation that characterizes aging is triggered by senescent cells and is intimately related to age-related diseases such as cardiovascular diseases and cancer.
“Of note, the local low-grade inflammation that characterizes aging is triggered by senescent cells and is intimately related to age-related diseases such as cardiovascular diseases and cancer (5, 291, 292).”
From IL-6 in inflammation, autoimmunity and cancer (2021) · cites this paper as [292]
The section “Aging is characterized by chronic low-grade inflammation” links inflammaging to age-related diseases, including cardiovascular disease and cancer. Box 4 says senescent cells may contribute to chronic inflammation through their pro-inflammatory secretions, while “Where do the stimuli fuelling inflammaging come from?” emphasizes cellular debris and altered self-molecules. The claim overstates the evidence by saying the inflammation is triggered by senescent cells. (LLM, conf=0.88)
Experimental — accuracy not yet measuredModulating the body's inflammatory balance is expected to increase longevity and reverse or mitigate age-related disease processes.
“modulating the body’s inflammatory balance is expected to increase longevity and reverse or mitigate age-related disease processes.472–474”
From Antiageing strategy for neurodegenerative diseases: from mechanisms to clinical advances (2025) · cites this paper as [472]
Systemic chronic inflammation is typically triggered by damage-associated molecular patterns without an acute infectious insult or pathogen-associated molecular pattern activation.
“In contrast, SCI is typically triggered by DAMPs in the absence of an acute infectious insult or activation of PAMPs30–32.”
From Chronic inflammation in the etiology of disease across the life span (2019) · cites this paper as [30]
Systemic chronic inflammation often increases with age, as older individuals have higher circulating cytokines, chemokines, acute phase proteins, and inflammatory gene expression.
“SCI often increases with age30, as indicated by studies showing that older individuals have higher circulating levels of cytokines, chemokines and acute phase proteins, as well as greater expression of genes involved in inflammation1,19,30.”
From Chronic inflammation in the etiology of disease across the life span (2019) · cites this paper as [30]
When combined with low physical activity, eating hyperpalatable processed foods high in fat, sugar, salt and flavor additives can trigger major shifts in cell metabolism, leading to greater production and faulty disposal of dysfunctional organelles such as mitochondria, and to misplaced, misfolded and oxidized endogenous molecules.
“when combined with low physical activity, consuming hyperpalatable processed foods that are high in fat, sugar, salt and flavor additives147 can cause major changes in cell metabolism and lead to the increased production (and defective disposal) of dysfunctional organelles such as mitochondria, as well as to misplaced, misfolded and oxidized endogenous molecules30,60,148”
From Chronic inflammation in the etiology of disease across the life span (2019) · cites this paper as [30]
These altered molecules increase with age and can act as DAMPs that innate immune cells detect, activating the inflammasome machinery, amplifying inflammation, and contributing to inflammaging.
“These altered molecules, which increase with age19,30, can be recognized as DAMPs by innate immune cells, which in turn activate the inflammasome machinery, amplify the inflammatory response1,30,60 and contribute to a biological state that has been called “inflammaging,””
From Chronic inflammation in the etiology of disease across the life span (2019) · cites this paper as [30]
According to the antagonistic pleiotropy theory of ageing, inflammation might have been evolutionarily selected for early-life benefits but becomes detrimental in old age.
“According to the antagonistic pleiotropy theory of ageing, inflammation might have been evolutionarily selected because of beneficial effects early in life and in adulthood, although it becomes detrimental in old age when the effect of natural selection is no longer active8.”
From Inflammageing: chronic inflammation in ageing, cardiovascular disease, and frailty (2018) · cites this paper as [8]
Pathobionts are enriched in the gut of older adults and are primarily dominated by facultative anaerobes such as Fusobacterium and Staphylococcus, a state associated with increased plasma inflammatory cytokines.
“This category of microorganisms is enriched in the gut of older adults and is primarily dominated by facultative anaerobes — such as Fusobacterium and Staphylococcus — a state that has been associated with increased levels of inflammatory cytokines in plasma8,70.”
From Inflammageing: chronic inflammation in ageing, cardiovascular disease, and frailty (2018) · cites this paper as [8]
There are no standard biomarkers for chronic inflammatory state, and studies have generally produced conflicting results.
“Despite the importance of this type of inflammatory reaction, there are currently no standard biomarkers to characterize a chronic inflammatory state and studies have generally yielded conflicting results18,19.”
From An inflammatory aging clock (iAge) based on deep learning tracks multimorbidity, immunosenescence, frailty and cardiovascular aging (2021) · cites this paper as [18]
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“Of note, the local low-grade inflammation that characterizes aging is triggered by senescent cells and is intimately related to age-related diseases such as cardiovascular diseases and cancer (5, 291, 292).”
BackgroundInflammation and aging: signaling pathways and intervention therapies
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Self-citationYoung bone marrow transplantation preserves learning and memory in old mice
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Mineralocorticoid receptor promotes cardiac macrophage inflammaging
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Inflammaging and Cardiovascular Risk in Old Women
Moscucci, F., Baratta, F., Bucciarelli, V., Mattioli, A. V., Pinti, M., Zanini, G., Sciomer, S., Gallina, S., Piccirillo, G., & Desideri, G. (2025) · High Blood Pressure & Cardiovascular Prevention · doi:10.1007/s40292-025-00758-1 · Cited by 8 · see citing works
- Authors
- Franceschi, C., Garagnani, P., Vitale, G., Capri, M., & Salvioli, S.
- Affiliations
- University of Bologna (IT)
- University of Milan (IT)
- Corresponding author
- Capri, Miriam
- Venue
- Trends in Endocrinology & Metabolism
- Publisher
- Elsevier BV
- Published
- 2017-03
- Volume
- 28
- Issue
- 3
- Pages
- 199-212
- ISSN
- 1043-2760 (ISSN-L)
- OpenAlex
- W2532576306
- Cited by
- 997
- References
- 112
- Citations by year
- 2026: 98 · 2025: 118 · 2024: 120 · 2023: 99 · 2022: 122 · 2021: 138 · 2020: 106 · 2019: 86 · 2018: 66 · 2017: 38 · 2016: 3 · 2013: 1
- FWCI
- 6.50
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Trends in Endocrinology and Metabolism (publishedVersion)
- PubMed (publishedVersion)
- Archivio istituzionale della ricerca (Alma Mater Studiorum Università di Bologna) (submittedVersion, cc-by-nc-nd)
- Funders
- EU Joint Programme – Neurodegenerative Disease Research
- European Commission (266486, EU-FP7, H2020, 634821)
- Università di Bologna
- Horizon 2020 Framework Programme (634821)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Life Sciences › Immunology and Microbiology › Immunology › Phagocytosis and Immune Regulation
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Clinical Biochemistry › Advanced Glycation End Products research
- Keywords
- inflammaging, aging, low-grade inflammation, macrophages, gut microbiota, cell debris, innate immune receptors, autophagy, mitophagy, proteasome, autoimmunity, chronic disease
- MeSH terms
- Animals, Autophagy, Humans, Inflammation, Mitochondria, Proteasome Endopeptidase Complex
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