Aging remodels mouse neutrophils across organs to drive inflammatory and senescence responses
Single-cell profiling reveals distinct neutrophil subsets that promote senescence in vascular and liver cells while altering bone marrow progenitor states.
Aging cell · Wang Y et al. · Paper published 30 Sep 2026
In mice, aging alters neutrophil abundance and cellular states across multiple organs, according to single-cell RNA sequencing analyses. Researchers mapped tissue-specific changes by comparing young and aged animals, identifying neutrophil subsets with elevated inflammatory, complement, oxidative stress, and IL-6 signaling signatures. These aged immune cells also influenced surrounding tissues. In cell culture assays, exposure to conditioned media from aged mouse neutrophils or IL-6-stimulated neutrophil-like cells induced inflammatory and senescence-associated responses in vascular smooth muscle cells and hepatocyte-derived cells. In the bone marrow, single-cell profiling showed age-related shifts in progenitor populations, including the expansion of an HPC11 progenitor subset marked by heightened myeloid priming. Computational perturbation analyses further nominated candidate regulators of these progenitor programs.
Why it matters
The findings establish a multi-organ atlas of neutrophil aging, highlighting how specific innate immune subsets directly promote tissue inflammation and cellular senescence across the body.
Caveats
The findings are based entirely on mouse datasets and in vitro cell culture, meaning these neutrophil dynamics require direct validation in human aging.
Written from the paper’s abstract, and every claim checked against it before publishing. Read the paper for the full methods and data.
The paper
Single-Cell Mapping Identifies Aging-Associated Neutrophil Remodeling Across Multiple Organs
Wang Y, Chang T, Fu Y et al.
Aging cell · 30 Sep 2026 · Peer-reviewed
- Relevance
- Core geroscience
- News value
- Notable
- Evidence
- Animals
- Status
- Peer-reviewed
More on Inflammaging
See allCranial bone marrow monocytes drive brain injury inflammation and respond to fenofibrate
Targeting PPARα deficiency in cranial bone marrow monocytes improved cognitive function and reduced neurodegeneration markers in older patients with chronic brain injury.
Science translational medicine · Lu Z et al.
Somatic blood mutations associate with accelerated frailty and functional decline in humans
In a preprint analyzing over 730,000 adults, researchers linked clonal hematopoiesis to faster physical decline mediated by T-cell changes.
medRxiv · Zhao K et al.
Impaired glymphatic clearance links inflammation to accelerated brain aging in schizophrenia
Neuroimaging and post-mortem transcriptomics connect disrupted astrocytic aquaporin-4 polarization and blood-brain barrier breakdown to increased epigenetic and brain age.
bioRxiv · Tan X et al.
ASXL1 mutations in clonal hematopoiesis accelerate aortic valve calcification
Large human cohort data and cell experiments show that ASXL1-driven clonal hematopoiesis worsens aortic valve hemodynamics and promotes calcification through inflammatory signaling.
medRxiv · Small A et al.
Loss of SATB1 alters 3D genome architecture in aged mouse T cells
Declining levels of the chromatin organizer SATB1 disrupt genomic boundaries and drive inflammatory gene activation in naive CD4+ T cells.
Science advances · Wang B et al.