A transitional senescence program drives inflammatory monocyte state expansion in aging humans
bioRxiv preprint, not peer-reviewed. Human monocyte data with small single-cell cohort; correlative sepsis link.
Evidence
3/10
Emerging Evidence
Sample
66
subjects
Duration
—
study period
Journal
bioRxiv (preprint)
Sep 2026
Full Abstract
Multiomic profiling of SA-bGal-sorted human monocytes proposing a transitional senescence-like bridge to an inflammatory state.
Key Findings
- 01
Variance of SA-bGal higher in older donors; mean not significantly different
- 02
Pseudotime suggests bridge from classical monocytes to inflammatory state; AP-1 dynamics
- 03
Older-donor monocytes ~2.2-fold enriched in sepsis-associated MS1 state
Structured Methods
- Study Design
- Preprint
- Sample Size
- 66 subjects
- Study Duration
- Not reported
- Methodology
- Flow cytometry, bulk RNA/ATAC-seq, single-cell multiome
- Limitations
- Preprint. Single-cell multiome only 4 young/3 older donors; trajectory inference and sepsis links correlative; AP-1 not tested experimentally in reviewed portions; posting date inferred from DOI.
Citations & References
Vasilopoulos T, Turano PS, Garza-Martinez L, Akbulut E, Konda M, Herbig U, et al. (2026). A transitional senescence program drives inflammatory monocyte state expansion in aging humans. bioRxiv (preprint). https://doi.org/10.64898/2026.09.09.750459
Sample member
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