By IANS,
Washington : Researchers now have a clearer, if more complicated, picture of how one class of immune cells goes wrong when loaded with cholesterol.
Their study shows that when it comes to the development of atherosclerosis, (thickening of artery walls) and heart disease, it’s not about any one bad actor – it’s about a network gone awry.
The new findings also highlight a pretty remarkable thing, says Jay W. Heinecke of the University of Washington (UW). “Despite 30 years of study, we still don’t know how cholesterol causes heart disease.”
But, with the new findings, scientists are getting closer. Earlier studies had shown that heart disease is about more than just high LDL (bad) cholesterol.
Cells known as macrophages also play a critical role. Macrophages are part of the innate immune system that typically gobble up pathogens and clear away dead cells.
But they also take up and degrade cholesterol derivatives.
When they get overloaded with those lipoproteins, they take on a foamy appearance under the microscope to become what scientists aptly refer to as foam cells.
Those foam cells are the ones that seem to have critical importance in the development of atherosclerosis.
People had typically thought about this problem in terms of linear pathways, Heinecke explained. In essence, macrophages end up with too much cholesterol going in and not enough coming out.
The macrophages get overwhelmed and trapped in the artery wall, and somehow plaques form as a result. But the new results show that it isn’t really about simple paths in and out; rather, there is an integrated network of macrophage proteins involved.
When that network gets disrupted, as it does when too much cholesterol comes in, atherosclerosis forms.
“It’s definitely a different way to think about what is going on,” Heinecke says, according to an UW release.
Heinecke’s group applied sophisticated technologies and statistical tools to get a global view of what happens to macrophage proteins when they turn into foam cells.
The findings were published in February issue of Cell Metabolism.