New insights into hibernation and clot prevention
Researchers from Ludwig-Maximilians-Universität Munich have revealed a surprising link between reduced activity of a protein called heat shock protein 47 and the ability of bears to hibernate without forming dangerous blood clots. The findings, published in a leading scientific journal, shed light on how long periods of inactivity can affect clotting risk in both animals and humans.
When people stay inactive for extended stretches—whether during illness, after surgery, or during long flights—they face a higher chance of developing blood clots in the legs. If these clots travel, they can reach the lungs or the brain, leading to pulmonary embolism or stroke. In contrast, bears survive months of dormancy without these clotting problems, suggesting natural mechanisms that protect against thrombosis during hibernation.
In the study, scientists measured a dramatic drop in HSP47 activity in hibernating bears. Specifically, the bears showed about a 55-fold reduction in HSP47 activity compared with periods of wakefulness. This stark change underscores a potential biological strategy that mitigates clot formation during extended rest.
Crucially, the researchers found that a similar phenomenon may occur in other species, including humans. Reduced HSP47 activity appears especially relevant for individuals who experience paralysis due to spinal cord injuries. This could explain why paralyzed people are not at higher risk of clots than their mobile peers under certain conditions. Yet, temporary inactivity, such as recovering from an injury or prolonged travel, can still raise clot risk for many people.
Current preventive measures for clot risk include medications like aspirin, but these can carry side effects, including a higher chance of bleeding. The discovery of HSP47 as a potential target opens the door to safer anti-clot therapies that could reduce complications without adding bleeding risks. Further work is needed to translate these findings into practical treatments and to understand how HSP47 regulation could be harnessed in clinical settings. (Attribution: Science journal, and related studies.)