Hibernating bears, paralyzed humans and pigs in small enclosures avoid dangerous blood clots despite being immobile for very long periods of time, a new study now explains why their blood does not lose its fluidity. A study by the University…
Hibernating bears, paralyzed humans and pigs in small enclosures avoid dangerous blood clots despite being immobile for very long periods of time, a new study now explains why their blood does not lose its fluidity.
Research from the University of Reading (United Kingdom), with colleagues from Denmark, Germany, Norway and Sweden, shows that a lack of a key protein prevents blood clotting in three species of mammals when they are frozen for days, weeks or weeks. Live , months or even years continuously.
When people fly long distances, they often follow advice to prevent dangerous blood clots (deep vein thrombosis) from forming in one or both legs while sitting for many hours. They may have reminders to get up and walk and even wear compression socks to prevent blood from pooling in the legs.
Most people don’t get a blood clot if they take care of themselves on an airplane, but genetic factors put some people at a serious risk of blood clots.
The discovery that a protein known as Hsp47 is dramatically reduced 55-fold when a person is sedentary for longer periods of time than in flight has led to new research to help people with inherited blood clotting disorders. Medications can build up that puts them at risk of pulmonary embolism. , heart attack, and stroke.
“It seems that severely paralyzed people are not at risk of blood clots. This tells us that something interesting is happening. And it turns out that reducing Hsp47 levels plays an important role in clot prevention.” , not just humans, but also in other mammals including bears and pigs,” said Professor John Gibbins, who led the work at the University of Reading.
Hsp47 is released by platelets, the sticky blood cells that trigger blood clotting. Normally, clotting is an important response to injury to prevent blood loss, and Hsp47 is one of the essential ingredients for platelets to do their job. Investigating Hsp47’s role in clotting, the team found that when released into the blood of bears, mice and humans, it promoted conditions that could lead to deep vein thrombosis.
“When we see something like this in multiple species, that reinforces its importance. Having Hsp47 must have been an evolutionary advantage,” Gibbins said. Keeps Hsp47 at an appropriate level. It may be that the mechanical forces involved in movement affect gene expression, leading to a drastic increase in the amount of Hsp47 in the blood.
This new discovery, published in the journal Science, could make it possible to protect people who get clots in the future. “Now that we know that Hsp47 is so important, we can begin to look for new or existing drugs that can block this protein’s role in blood clotting and protect those who are mobile and prone to clots.” are afflicted.”
