A molecular signal keeps blood cells young
As we age, our blood-making system weakens. Researchers have now identified a single molecular brake that drives that decline and shown it can be released, with striking effects on blood cell production.
The production of blood cells (haematopoiesis) declines with age. The consequences are real: fewer red blood cells, a diminished immune response, and greater vulnerability to infection and anaemia. A new study published in Nature Aging pinpoints a specific mechanism driving that decline: damage signals emanating from shortened chromosome tips, known as telomeres.
Silencing the damage signal restores function
Telomeres are protective caps at the end of every chromosome. They shorten each time a cell divides. When they become critically short, they trigger a distress signal that tells the cell to stop dividing. This is normally protective, preventing damaged cells from proliferating. But in blood-forming stem cells (haematopoietic stem cells), that same signal also suppresses the production of healthy blood cells.
The researchers tested whether they could suppress this damage signal by targeting non-coding RNA molecules associated with telomeres (telomeric RNA). The approach worked. In mice lacking the enzyme that maintains telomere length (telomerase-deficient mice), and in normally aged wild-type mice, the treatment restored blood cell production. Human haematopoietic stem cell function also improved in laboratory settings. These findings are reported by the researchers in their publication.
What this means for immune ageing
The findings are preliminary and partly derived from animal models. Whether the same approach is effective and safe in humans has not yet been established. The direction is nonetheless notable. Much of the immune system’s decline in older age traces back to a shortage of well-functioning stem cells in the bone marrow. If telomere damage signals impair those stem cells, suppressing them represents a plausible therapeutic avenue. The study adds a concrete mechanism to our understanding of blood cell ageing and is relevant to research on immune ageing (immunosenescence).
Search terms to explore further: telomere DNA damage signalling, haematopoietic stem cell aging, immunosenescence bone marrow