⚠️ Auto-extracted by Claude on 2026-06-13 — closed-access (Cell Press / Molecular Cell); claims sourced exclusively from the verified metadata and the verbatim PubMed abstract. Full text not read. Do NOT rely on quantitative specifics until a full-text verification pass. gap/no-fulltext-access
Anerillas et al. 2026 — SenCat: cataloging human cell senescence by multi-omic profiling (SenNet)
Molecular Cell, online ahead of print 11 June 2026. doi:10.1016/j.molcel.2026.05.017 · PMID:42276073. A NIH SenNet consortium data paper from the NIA Intramural Research Program (Gorospe / Basisty labs); a companion to the SenNet Perspective suryadevara-2026-senotypes.
Access: Closed-access (Cell Press). Abstract-sourced only. gap/no-fulltext-access
What this paper is
A primary multi-omic data paper — not a review. It builds “SenCat,” a catalog of human cellular senescence assembled by profiling the transcriptomes and proteomes of 14 different primary human cell types induced into senescence across >30 senescence paradigms (different inducers/conditions).
Findings (abstract-supported)
- No single universal senescence marker. Senescent cells from all 14 primary cell types did not share one unique marker — direct empirical support for senescent-cell heterogeneity (the “senotype” concept; see cellular-senescence § Senescent-cell heterogeneity and the senotype concept). This is the catalog-scale confirmation that single-marker approaches (p16, SA-β-gal alone) cannot capture the full senescent population.
- Shared repair-associated pathways despite marker divergence. Across cell types, senescent cells activated shared specific metabolic and damage-response pathways implicated in tissue repair — i.e., a common functional core exists beneath the marker heterogeneity.
- A machine-learning-refined composite signature. ML-refined SenCat signatures enabled senescence scoring and identification across multiple human and mouse datasets, at both bulk and single-cell resolution — a usable senescence classifier where individual markers fail.
Significance for the wiki
- Resolves “is there a universal senescence marker?” → NO (across 14 primary human cell types / >30 paradigms). This is the strongest peer-reviewed grounding for the senotype-heterogeneity claim that the suryadevara-2026-senotypes Perspective frames and the Krizhanovsky preprints (cherqui-2025-senescence-burden-organs, freizus-2025-atp6v1b2-persistent-senescence) corroborate.
- A composite, multi-cell-type senescence signature (SenCat) is a candidate scoring tool — relevant wherever the wiki notes the absence of a validated single senescence biomarker (see sasp § Limitations and gaps).
- The shared metabolic + damage-response/repair pathways point is a constructive counterpoint to pure heterogeneity: there is a conserved functional senescence core, even if no single marker is universal.
Cross-references
- cellular-senescence — primary atomic home; senotype heterogeneity section
- suryadevara-2026-senotypes — companion SenNet Perspective (senotype framework)
- sasp — SASP composition + the no-validated-single-biomarker gap
- hallmarks-of-aging — parent framework