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Seven studies by Mayo Clinic researchers examine how senescent cells vary across tissues, contribute to inflammation and could be targeted or measured. Some interventions showed encouraging results in older mice, but their safety and effectiveness in people have not been established.
Mayo Clinic researchers have published seven studies examining how senescent cells vary across tissues, drive inflammation and might be targeted, adding findings to a broader effort to map these cells in the human body. The work includes experimental treatments that showed encouraging effects in older mice, but it does not establish that the approaches are safe or effective in people.
Senescent cells stop dividing but do not simply disappear. They can remain active and release inflammatory substances, a pattern associated with diseases linked to aging. The Mayo studies, conducted by scientists at the Robert and Arlene Kogod Center on Aging and published in Nature journals, investigate how to identify different senescent cell populations and understand the processes behind their effects.
One study developed SenMayo, a gene set that uses patterns of gene activity to help identify senescent cells across tissues and experimental systems. Researchers tested it with bone biopsies from older adults and reported that its gene signature became less prominent after senescent cells were removed in preclinical experiments. The resource has since been used by other researchers, according to the source report.
Other studies examined links between malfunctioning mitochondria and inflammation. The researchers reported that mitochondrial DNA and RNA can activate immune responses, and that changes in mitochondrial metabolism can affect inflammatory gene activity through epigenetic mechanisms. These findings point to possible ways of reducing some inflammatory signals without eliminating the senescent cells themselves.
The team also tested senolytic medications, a natural compound found in tomatoes and genetic methods aimed at particular cell populations. In older mice, the approaches were associated with changes including reduced inflammatory measures and improvements in selected outcomes related to frailty, brain inflammation and cognitive-task performance. A separate study identified IL-23R as a potential biomarker in blood and tissue. The report describes it as a candidate for further study, not an established test of biological age or treatment success.
The findings address a basic problem in aging research: senescent cells are not a single, uniform target. Their features differ according to where they occur and the processes that caused them to stop dividing. More reliable ways to recognize distinct cell populations could help researchers test whether a treatment affects the cells linked to a particular disease or tissue, rather than treating all senescent cells as alike.
The work also broadens the range of strategies under investigation. Rather than only trying to remove senescent cells, researchers may be able to interrupt pathways that make them release inflammatory signals. If those mechanisms can be safely targeted, they could inform future research into age-related conditions. That possibility remains a research direction; the mouse findings do not establish a human treatment or show that an intervention will extend life or prevent disease.
The proposed IL-23R biomarker could also be useful if further studies show it reliably tracks relevant changes in people. A dependable measure could help researchers assess biological processes and evaluate candidate treatments, but the current report does not establish its clinical use.
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SenNet’s Nationwide Cell-Mapping Effort
The Mayo studies contribute to the Cellular Senescence Network, or SenNet Consortium, a U.S. research effort supported by the National Institutes of Health Common Fund. Its aim is to document where senescent cells appear in different tissues and how they change over a person’s lifetime. Mapping those differences may help explain why the cells have different effects in different settings.
Identifying senescent cells has been difficult because no single feature necessarily captures every cell type. The SenMayo gene set offers researchers a shared method based on gene activity, while the studies of mitochondrial signaling examine possible reasons some senescent cells sustain inflammatory activity. Together, the work moves from recognition toward understanding how particular cell populations behave.
The findings were led by multiple researchers. Mayo endocrinologist Sundeep Khosla was senior author of the SenMayo study. João Passos was senior author of three papers on senescent cell diversity and mitochondrial mechanisms. Marissa Schafer led studies on the IL-23R biomarker and targeting senescent cells in aged mouse brain tissue.
“This body of work is moving the aging field forward to precisely identify, understand and target the specific senescent cells that contribute to age-related dysfunction, which is the necessary groundwork to develop new therapies that support healthy aging.”
— Marissa Schafer, Ph.D., Mayo Clinic scientist
Human Safety and Benefits Remain Unknown
The reported intervention results are from older mice; the source material does not report clinical trial results in people. It remains unclear whether the treatments would produce similar effects in humans, what risks they might carry, or which patients could benefit. The findings do not support using senolytic drugs or the tomato-derived compound as anti-aging treatments outside properly designed research.
The report also does not specify the size of each experiment, the magnitude of the observed effects or how long the outcomes lasted. It does not establish whether the IL-23R candidate can distinguish aging-related changes from other biological processes, or whether it could guide treatment decisions. Those questions require further study.
Although SenMayo was tested using human bone biopsies, that does not mean the experimental interventions have been validated in people. The studies add evidence about cell identification and biology, while clinical effectiveness remains unconfirmed.
Further Tests Before Human Treatments
The next steps are additional research to test whether the proposed cell markers and mitochondrial pathways hold up across tissues and conditions, and to determine which interventions can be developed safely. For the potential treatments, that includes establishing effects and risks beyond the mouse experiments before drawing conclusions about human use.
Researchers in the SenNet Consortium are working to map senescent cells across the body and over the course of life. That effort may provide a wider reference for comparing cell populations and evaluating future studies. The Mayo report gives no timetable for clinical trials or for use of IL-23R as a medical test, so those milestones remain uncertain.
Key Questions
What are senescent, or “zombie,” cells?
They are cells that have stopped dividing but remain active. Some release inflammatory substances that researchers associate with age-related dysfunction.
Did the Mayo Clinic studies prove a treatment works in people?
No. The reported treatment findings came from experiments in older mice. The source report says further research is needed to establish safety and effectiveness in people.
What is the SenMayo gene set?
It is a tool based on patterns of gene activity that researchers developed to identify senescent cells more consistently across tissues and experimental systems.
What is IL-23R’s proposed role?
The researchers identified IL-23R as a potential blood and tissue biomarker linked to senescence. It has not been established as a clinical test for biological age or treatment response.
What happens next for the research?
Researchers must test the findings further, including whether the experimental approaches are safe and effective in people. The SenNet Consortium is also continuing its effort to map senescent cells across tissues and over a person’s lifetime.
Source: sciencedaily.com
