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As we age, our bones become weak and brittle, a process called osteoporosis. This bone loss is caused by changes in the cells within the bone marrow microenvironment, such as elevated fat and inflammation-promoting immune cells. One molecular driver of inflammation is the STING signaling pathway, though the role of this pathway in aging bones has until now been unclear.

In a new study, published in Advanced Science, researchers discover that the STING pathway is activated in bone marrow macrophages during aging and could be a target to prevent bone loss.

The STING pathway is part of the innate immune system, sensing and protecting against infection, cellular stress and cancer. The researchers found that this pathway is increasingly activated in bone marrow macrophages with age. Bone marrow macrophages (BMMs) are immune cells that protect against pathogens and can increase inflammation, a hallmark of skeletal aging.

The researchers investigated the STING pathway with mice lacking the STING protein in bone marrow cells. Surprisingly, at a young age, mice lacking STING showed reduced bone density, but later in life, mice lacking STING were protected against bone loss.

To determine what activated the STING pathway in BMMs, the researchers turned to a different bone marrow cell: fat cells , called bone marrow adipocytes (BMAds). By isolating BMAds from older mice and culturing them with BMMs from young mice, they found that BMAds promoted STING activation in BMMs.

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