An NIH-funded consortium has published the first broad atlas of senescent cells across human tissues and introduced a classification framework for cells that stop dividing but remain biologically active.
The Cellular Senescence Network, or SenNet, presented the work in a group of papers published June 11 in Cell. NIH launched the Common Fund program in 2021 because senescent cells are rare, diverse and difficult to identify in complex tissue.

Senescent cells are not uniformly harmful. They can support wound healing and help suppress tumors, while cells that accumulate with age can release inflammatory signals associated with chronic disease and other age-related changes.
The researchers call their new groupings 'senotypes.' The framework distinguishes cells according to tissue, health status and surrounding conditions, with the aim of preserving useful functions while identifying harmful subtypes for further study.
The atlas includes tissue maps from the brain's prefrontal cortex, lungs and lymph nodes. Consortium teams combined single-cell measurements, spatial methods, computational tools and artificial intelligence to detect cellular features.
NIH also reported blood markers associated in aging studies with kidney disease, frailty and future diabetes risk. Those research associations are not a clinical test recommendation and do not establish that the markers cause those outcomes.

The program is exploring experimental senolytics, drugs intended to remove selected senescent cells. The atlas is foundational research, however; it does not show that an approved therapy can safely target a senotype in patients.
Because the atlas spans multiple teams, tissues and measurement methods, definitions and validation will matter as the resource grows. A cell classified in one experimental setting may require confirmation in other populations and laboratories.
The immediate advance is a public research framework: scientists can ask where distinct senescent states occur and how they differ instead of relying on a single marker or assuming every nondividing cell has the same role.
