Proposed Aging Purinome framework links purinergic signaling to inflammaging
The authors propose the Aging Purinome as a framework for how age-associated changes in extracellular purinergic signaling may contribute to chronic low-grade inflammation, called inflammaging. [1]
Automatic summary · not editorially reviewed
The key findings
The authors propose the Aging Purinome as a systems-level framework for age-associated remodeling of extracellular purinergic signaling. [1]
Reported evidence indicates aging alters extracellular ATP availability and causes receptor-, cell- and tissue-specific changes in P2X and P2Y receptors. [1]
Exercise, nutritional approaches and pharmacological modulation of purinergic and NAD+-related pathways are examined as potential strategies. [1]
The source at a glance
- Study type / format
- Proposed conceptual framework (abstract)
- Population / context
- Aging biology and extracellular purinergic signaling, described at a conceptual level
- Summary based on
- Study abstract
- Original publication
- October 10, 2026
Proposed framework for age-related purinergic remodeling
Aging involves a progressive decline in cellular homeostasis together with chronic, low-grade sterile inflammation, called inflammaging. The authors state that the molecular networks linking the hallmarks of aging to this inflammation remain incompletely understood. They therefore propose the Aging Purinome as a systems-level framework. It describes progressive, age-associated remodeling of extracellular purinergic signaling and its metabolic interfaces. The network includes extracellular nucleotides and nucleosides, release and transport mechanisms, ectonucleotidases, P2X and P2Y receptors, adenosine receptors and interconnected metabolic pathways. This is a proposal, not a validated product or test.
Supporting source [1]
Reported age-related changes and the P2X7-NLRP3 example
According to the available evidence cited, aging alters extracellular ATP availability. It also produces receptor-, cell- and tissue-specific changes across the P2X and P2Y receptor repertoire. The authors further report dysregulation of the CD39-CD73-adenosine axis and increased CD38-dependent NAD+ consumption. Among these pathways, P2X7-NLRP3 signaling is described as a well-characterized mechanism linking extracellular ATP to sterile inflammation. The authors stress that it is only one component of a broader purinergic remodeling process. They discuss how these changes may influence mitochondrial dysfunction, cellular senescence, altered intercellular communication, impaired inflammatory resolution and age-related diseases. These are discussed possibilities, not demonstrated causes.
Supporting source [1]
Potential strategies and abstract-only scope
The authors examine exercise, nutritional approaches and pharmacological modulation of purinergic and NAD+-related pathways as potential strategies to restore homeostatic signaling. They present the Aging Purinome as a testable basis for future mechanistic and translational studies. This text is an abstract; the full text was not reviewed. The abstract does not report study design, sample, follow-up or measured outcomes, so no effect sizes or human benefits can be stated. Associations and proposed mechanisms are not causes, and the strategies are not recommendations.
Supporting source [1]
How to interpret this
Abstract only; the full text was not reviewed. No study design, sample, follow-up or measured outcomes are reported, so no effect sizes or human benefits can be stated. The framework is a proposal, and discussed mechanisms and strategies are not established causes or recommendations.
Based on the study abstract; the full paper, tables and supplementary data were not reviewed.
Source & supporting passages
Ozelame BC, Cardoso AM, Manica A. · europepmc.org · October 10, 2026