Narrative review: immune aging and metabolic disease at the immunometabolic interface
This narrative review, informed by a structured literature search, examines links between immune aging and metabolic dysfunction and evaluates inflammaging as a central process at this interface. It stresses that direction, reversibility and modifiability of these relationships in humans remain incompletely resolved. [1]
Automatic summary · not editorially reviewed
The key findings
Aging is described as associated with immune remodeling: reduced protective capacity plus persistent low-grade inflammation, discussed as immunosenescence and inflammaging. [1]
The review discusses how age-related immune remodeling may contribute to insulin resistance and metabolic impairment across several tissues, and how metabolic stress may promote features of immune aging. [1]
The review states that the direction, reversibility and modifiability of these relationships in humans remain incompletely resolved. [1]
The source at a glance
- Study type / format
- Narrative review informed by a structured literature search (abstract only)
- Population / context
- People affected by aging-related metabolic disorders such as obesity, type 2 diabetes, metabolic dysfunction-associated steatotic liver disease and cardiovascular complications, as framed in the review.
- Summary based on
- Study abstract
- Original publication
- October 1, 2026
Review distinguishes immune-aging concepts and pathways
The authors describe aging as associated with broad remodeling of the immune system: reduced protective capacity together with persistent low-grade inflammatory activity, discussed as immunosenescence and inflammaging. They first distinguish related but non-identical concepts: immunosenescence, inflammaging, metaflammation, cellular senescence and the senescence-associated secretory phenotype. They then summarize core pathways involving NF-κB, NLRP3, mTOR, AMPK, insulin/IGF-1 and JAK/STAT signaling. These are described as mechanisms under discussion, not as established causes of human metabolic disease.
Supporting source [1]
Possible links across tissues, in both directions
The review discusses how age-related immune remodeling may contribute to insulin resistance, tissue inflammation and metabolic impairment across adipose tissue, liver, skeletal muscle, pancreatic islets, vasculature and the gut barrier. It also considers the reverse direction: how hyperglycemia, lipotoxicity, mitochondrial stress and epigenetic reprogramming may promote selected features of immune aging. The wording is cautious throughout; these are proposed links, and the review does not establish that immune aging causes metabolic disease.
Supporting source [1]
Biomarkers, heterogeneity and candidate strategies in review
The authors further review emerging biomarker domains, major sources of biological heterogeneity, and candidate therapeutic strategies, including lifestyle interventions, senescence-targeting approaches and metabolic modulators. They explicitly attend to evidence strength, translational limitations and clinical risk-benefit considerations. The review concludes that the immunometabolic interface offers a useful geroscience framework for understanding aging-related metabolic disease, while the direction, reversibility and modifiability of these relationships in humans remain incompletely resolved.
Supporting source [1]
How to interpret this
Abstract only; the full text was not reviewed. This is a narrative review informed by a structured literature search, not a primary study, so it reports no sample, follow-up or outcome data of its own. Proposed mechanisms and candidate strategies are discussed with attention to evidence strength and translational limits; the abstract does not establish causation or human benefit.
Based on the study abstract; the full paper, tables and supplementary data were not reviewed.
Source & supporting passages
Ziyu Ye, Lehua Yu, Ziran Li, Juan Huang, Bihua Lin, Bonan Xiang, Yanfang Liang, Jincheng Zeng · doi.org · October 1, 2026