Inflammaging: a new immune-metabolic viewpoint for age-related diseases.
Level 5 - mechanism / opinion, no new human data
Narrative review synthesizing conceptual and mechanistic models without primary empirical data or systematic review methodology.
PubMed 30046148 · doi:10.1038/s41574-018-0059-4
What was done
This narrative review synthesized mechanistic and evolutionary concepts linking chronic, sterile, low-grade inflammation (inflammaging) to metabolic inflammation (metaflammation) and age-related disease pathogenesis. The authors evaluated the roles of innate immune sensing, non-self, self, and gut microbiota (quasi-self) triggers, and discussed multi-omic biomarkers (DNA methylation, glycomics, metabolomics, lipidomics) for evaluating biological versus chronological aging.
What was found
The abstract provides conceptual arguments rather than empirical or quantitative data. The authors propose that inflammaging and metaflammation operate through shared innate immune receptor pathways sensing cellular debris, pathogens, and nutrient excess. They identify the gut microbiota as a central modulator linking metabolism and inflammation, argue that chronic diseases actively accelerate the biological aging process, and propose multi-omic profiling to quantify this acceleration.
Why it matters
It unifies metabolic dysfunction and age-related chronic diseases under a shared immunometabolic framework, highlighting biological aging biomarkers as potential tools to monitor disease progression.
Limits
The abstract describes a narrative theoretical framework without primary experimental data, systematic literature search methodology, or quantitative effect sizes. Clinical utility and validity of the proposed biomarker panels are discussed conceptually rather than evaluated systematically.
Cited by
- supports The term 'inflammaging' was coined by Italian researcher Claudio Franceschi to describe low-level, sterile, chronic inflammation associated with aging.