Mouse multi-organ single-cell map of aging-associated neutrophil remodeling
In mice, single-cell data from several organs showed organ-dependent shifts in neutrophil numbers and states with aging, plus inflammatory and IL-6-related programs; cell-culture and computational results are candidates, not proven human effects. [1]
Automatic summary · not editorially reviewed
The key findings
The study integrated single-cell RNA sequencing datasets from multiple organs of young and aged mice. [1]
Neutrophil subsets were enriched for inflammatory, oxidative stress, complement and IL-6-related transcriptional programs. [1]
A computational perturbation analysis nominated candidate regulators of subtype-specific transcriptional programs. [1]
The source at a glance
- Study type / format
- Abstract of a multi-organ single-cell RNA sequencing dataset-integration study with cell-culture and computational analyses in mice
- Population / context
- Young and aged mice; mouse neutrophils, bone marrow progenitors and cultured vascular smooth muscle and hepatocyte-derived cells.
- Summary based on
- Study abstract
- Original publication
- October 1, 2026
Young and aged mice, multiple organs, single-cell data
The abstract describes an analysis that combined single-cell RNA sequencing datasets from multiple organs of young and aged mice. The aim was to characterize how neutrophils change with aging, since their role and varied states were described as incompletely understood. This is an abstract of a mouse dataset-integration study; the full text was not reviewed.
Supporting source [1]
Organ-dependent neutrophil shifts and inflammatory programs
The analysis found organ-dependent changes in neutrophil abundance and in the mix of neutrophil states. Some neutrophil subsets were enriched for inflammatory, oxidative stress, complement and IL-6-related transcriptional programs. In cell culture, medium from neutrophils of aged mice, or from IL-6-stimulated neutrophil-like cells, increased inflammatory and senescence-associated responses in vascular smooth muscle and hepatocyte-derived cells. These are cell-culture observations, not evidence of effects on human lifespan.
Supporting source [1]
Bone marrow progenitors and computationally nominated regulators
Single-cell analysis of bone marrow showed aging-associated shifts in progenitor composition and transcriptional states, including an old-enriched HPC11 population with enhanced myeloid priming. A computational perturbation analysis nominated candidate regulators of subtype-specific transcriptional programs. The abstract calls these candidate neutrophil states and potential signaling axes associated with age-related inflammatory tissue environments; it does not establish causes or human treatments.
Supporting source [1]
How to interpret this
Abstract only; the full text was not reviewed. Findings come from mice, cell culture and computational analysis, so they do not show causes or benefits for human aging.
Based on the study abstract; the full paper, tables and supplementary data were not reviewed.
Source & supporting passages
Wang Y, Chang T, Fu Y, Liang G, Liu H, Zhang L, Yan J, Liu M, Liu A, Zhang C. · europepmc.org · October 1, 2026