What this means
Adipose tissue plays a key role in metabolic health, contributing to systemic dysfunction upon obesity or aging. A major driving factor of adipose-driven dysfunction is the accumulation of senescent cells (SnCs), but identification and characterization of specific SnCs is limited.
A plain-English summary is on its way. Until then, this is the start of the authors' own summary.
- Who it was tested in
- Not stated
- Kind of research
- Early results, not yet checked by other scientists
The science
- Original title
- Identification of an Endothelial Senotype Predicted by Ion Channel Expression in Aged Murine Perigonadal Adipose Tissue
- Authors
- Hertzel, A., Ali, S. S., Bartolomucci, A. et al.
- Journal
- bioRxiv (preprint, not yet peer reviewed)
- Published
- Oct 28, 2026
- Study type
- Preprint
Abstract
Adipose tissue plays a key role in metabolic health, contributing to systemic dysfunction upon obesity or aging. A major driving factor of adipose-driven dysfunction is the accumulation of senescent cells (SnCs), but identification and characterization of specific SnCs is limited. To identify age-dependent SnCs, we performed snRNA-Seq on young and old adipose using two independent analytical strategies. The first, a SenMayo-based approach and the second, dependent on SEAC guidelines and Pearson correlation identified senescent nuclei in endothelial clusters. Subsequent subclustering and cell-to-cell communication analyses identified endothelial capillary nuclei that overexpress macrophage migration inhibitory factor (Mif), which exemplifies the specific characteristics and microenvironment of SnCs. Finally, rank analysis identified ion channel transport genes as the most predictive of the SnCs. Overall, these results highlight new defining features of senescence in endothelial adipose tissue and provide novel age-dependent biomarkers.
Hertzel, A., Ali, S. S., Bartolomucci, A. et al. Identification of an Endothelial Senotype Predicted by Ion Channel Expression in Aged Murine Perigonadal Adipose Tissue. bioRxiv. 2026. doi:10.64898/2026.10.26.761925. https://doi.org/10.64898/2026.10.26.761925