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A study published in Advanced Science found that STING signaling in bone marrow macrophages was linked to age-related bone loss in mice. Removing STING from bone marrow cells protected older mice from bone loss, but reduced bone density when they were young; the findings do not establish a treatment for people.
Researchers have linked activity in the STING pathway to age-related bone loss in mice, identifying a possible target for future osteoporosis research. In a study published in Advanced Science, they traced a chain involving aging bone marrow fat cells, inflammatory macrophages and reduced NAD+, a molecule needed for normal cell functions.
The team found that STING signaling increased with age in bone marrow macrophages, immune cells that can contribute to inflammation. To test the pathway’s role, researchers studied mice lacking the STING protein in bone marrow cells. Those mice had lower bone density when young, but were protected against bone loss later in life, suggesting STING’s effects may vary with age.
To investigate what might activate STING, the researchers examined bone marrow adipocytes, or fat cells. In laboratory experiments, fat cells isolated from older mice promoted STING activation when cultured with macrophages from young mice. The team identified the protein DPP4, secreted by the fat cells, as a factor that activated STING and was associated with inflammation and bone loss.
The researchers also reported that STING activation was linked to NAD+ depletion in nearby bone marrow cells. Lower NAD+ impaired bone marrow stem cells’ ability to develop into cells that form and repair bone. The findings connect three cell types involved in skeletal aging, but the experiments described were conducted in mice and cell cultures.
The findings offer a potential explanation for how changes in the aging bone marrow environment may contribute to weakening bones. Rather than pointing to a single cell type, the study connects marrow fat cells, immune-cell signaling and stem-cell function in a sequence that could help researchers identify where age-related bone loss begins.
STING could be a research target because its activity appears to sit between signals from aging fat cells and changes that limit bone formation. But the results do not show that blocking STING is safe or effective as a way to prevent osteoporosis in people. The contrasting results in young and older mice also indicate that age and biological context matter when considering the pathway.
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How the Researchers Traced the Pathway
Osteoporosis involves bones becoming weaker and more vulnerable to fracture. The study focuses on changes in the bone marrow microenvironment, where fat cells, immune cells and cells that support bone formation interact. STING is part of the innate immune system, which responds to infection and other forms of cellular stress.
The paper, by Li and colleagues, was published by Wiley in Advanced Science in 2026. Its title is “Bone Marrow Macrophage STING Signaling is a Direct Nexus Linking Marrow Adipose Expansion to NAD+ Depletion and Osteogenic Decline in Skeletal Aging.” The experiments examined age-related changes in mice and laboratory cell cultures; the supplied report does not describe a human trial.
“The authors described STING signaling in bone marrow macrophages as a “pivotal integration hub.””
— The study authors
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Human Treatment Evidence Is Missing
The available findings do not establish whether the same DPP4-STING-NAD+ sequence drives bone loss in people. The report describes mouse and cell-culture experiments, not clinical testing, and does not show that a drug targeting STING prevents fractures or osteoporosis in humans.
It is also unclear how the pathway’s effects change across different ages, or what consequences long-term STING inhibition might have outside bone. The finding that young mice without STING had reduced bone density cautions against assuming that suppressing the pathway would benefit everyone. The study identifies a mechanism for further investigation, rather than a proven prevention strategy.
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From Mouse Findings to Human Studies
The next step is to establish whether the pathway is active in human bone marrow in comparable ways and whether its components are linked to bone loss over time. Further research would also need to test whether changing STING or DPP4 activity can preserve bone in relevant models without causing harmful effects elsewhere.
No clinical trial, treatment recommendation or timeline for human testing is reported in the source material. Until evidence from human studies is available, the findings should be understood as a preclinical research lead, not a basis for changing osteoporosis care. People with questions about bone health or treatment should consult a qualified health professional.
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Key Questions
What did the study find?
In mice and cell-culture experiments, researchers linked aging bone marrow fat cells and the protein DPP4 to STING activation in macrophages. They also connected this activity with inflammation, reduced NAD+ and impaired bone-forming capacity.
Did removing STING protect the mice?
Mice lacking STING in bone marrow cells had lower bone density when young but were protected against bone loss later in life. The results suggest its effects may differ with age.
Does this mean a STING-targeting drug can prevent osteoporosis?
No. The findings are from preclinical research and do not show that a STING-targeting treatment prevents osteoporosis in people or is safe for that use.
What role did DPP4 play?
The researchers identified DPP4 secreted by older-mouse bone marrow fat cells as a factor that activated STING in macrophages in their experiments. Its role in human osteoporosis remains unconfirmed.
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