Proposed modular framework for human cellular aging across organs and diseases
By projecting cell-type signatures onto plasma proteins from about 50,000 participants, the authors propose 14 cellular aging modules; accelerated epithelial aging was associated with disease burden and mortality. [1]
Automatic summary · not editorially reviewed
The key findings
Cell-type-enriched signatures were projected onto plasma proteins from about 50,000 participants across 128 organ–cell type pairs. [1]
The authors identified 14 cellular aging modules, and structural and tissue-resident modules remodeled earlier than immune lineages. [1]
Accelerated epithelial aging showed broad associations with disease burden and mortality. [1]
The source at a glance
- Study type / format
- Abstract of an integrative multi-organ single-cell and plasma proteomic study with longitudinal analyses
- Population / context
- Approximately 50,000 human participants with plasma proteomic profiles, plus a multi-organ single-cell transcriptomic atlas.
- Summary based on
- Study abstract
- Publication status
- Preprint · peer-review status not confirmed
- Original publication
- August 13, 2026
Single-cell atlas linked to plasma proteins
The authors combined a multi-organ human single-cell transcriptomic atlas with plasma proteomic profiles from approximately 50,000 participants. They projected cell-type-enriched molecular signatures onto circulating proteins to reconstruct cellular aging states at population scale. This approach covers 128 organ–cell type pairs. The abstract does not report how aging states were validated against independent measures.
Supporting source [1]
14 modules and earlier structural remodeling
The analysis identified 14 cellular aging modules: conserved cross-organ programs plus organ-specific aging states. Cellular identity emerged as a dominant organizing axis that transcends anatomical boundaries. Modules showed distinct temporal trajectories, with structural and tissue-resident modules remodeling earlier than immune lineages. Inter-individual heterogeneity was substantial: 34% of individuals showed extreme aging deviation in at least one cellular module.
Supporting source [1]
Disease associations and selective lifestyle links
Accelerated aging of specific modules, particularly epithelial aging, showed broad associations with disease burden and mortality. Longitudinal analyses reported stability and clinical relevance of cellular aging states. Lifestyle, metabolic and pharmacological factors showed selective relationships with individual aging programs. These are associations, not evidence that any factor causes or slows aging; the abstract gives no effect sizes, follow-up lengths or adjustment details.
Supporting source [1]
How to interpret this
Abstract only; the full text was not reviewed. The modular framework is proposed, not validated or approved for clinical use. Associations do not show causation, and no effect sizes, follow-up durations or adjustment details are reported.
Based on the study abstract; the full paper, tables and supplementary data were not reviewed.
Source & supporting passages
Guo J, Liu C, Yang X, Feng J, Wang J, Shi W, Yu X, Huang D, Dong S, Guo Y, Yang T. · europepmc.org · August 13, 2026