Human cell experiments found no universal senescence marker
Experiments across 14 human cell types and more than 30 senescence models found shared metabolic and damage-response pathways despite differences in individual markers.
Our read
AI & data- Studied:
- Experiments in primary human cells, against proliferating control cells
- What changed:
- No RNA or protein marker changed consistently across 14 human cell types compared with proliferating controls
- The catch:
- Fixed sampling times can miss transient senescence markers
Editor of record: Boris Djordjevic · AgingResearch.News
Fourteen types of human cells grown from tissue samples were used in lab experiments to build SenCat, a catalog of senescence, a state in which cells stop dividing. Researchers induced this state in more than 30 experimental models, using triggers including chemotherapy and radiation. They compared gene activity and proteins with those in control cells.
No single RNA or protein marker identified senescence across every cell type. Instead, the cells activated shared pathways involved in metabolism and responses to damage that are implicated in tissue repair. Machine learning combined multiple markers into scores that distinguished senescent cells from controls. The team also applied these signatures to human and mouse datasets to identify senescence in groups of cells and individual cells.
Why it matters
Studying senescence in aging tissues requires ways to recognize it across cell types. The authors propose considering shared pathways, rather than individual RNA molecules or proteins, as targets for approaches aimed at senescent cells.
Caveats
The catalog was built from lab-grown cells exposed to senescence triggers, rather than naturally aging human tissues. The reported mouse experiments used chemotherapy to induce senescence rather than studying natural aging.
From the paper
- Limitation
First, there is still a mismatch between transcriptomic and proteomic data across senescence models, reflecting a multi-leveled regulation of gene expression and making it difficult to define unified molecular signatures.
Quoted word for word from the full text on PubMed Central.
- Resources: datasets, atlases and tools
- Cellular senescence
- DNA damage response
- Senescence markers
- Humans
The paper
National Institutes of Health
Molecular Cell, Jun 11, 2026, Open access
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