atherosclerosis tagged posts

Columbia University researchers have found cells inside clogged arteries share similarities with cancer and aggravate atherosclerosis, raising the possibility that anticancer drugs could be used to treat atherosclerosis and prevent heart attacks.

Their study found that smooth muscle cells that normally line the inside of our arteries migrate into atherosclerotic plaques, change their cell identity, activate cancer genes, and proliferate inside the plaques.

“Our study shows that these transformed muscle cells are driving atherosclerosis, opening the door to new ways to treat the disease, potentially with existing cancer drugs,” says Muredach Reilly, MD, the Florence and Herbert Irving Endowed Professor of Medicine at Columbia University Vagelos College of Physicians and Surgeons ...

Deleting the TRPM2 protein from macrophages reduced atherosclerosis in mice. Macrophages travel through our arteries, gobbling fat. But fat-filled macrophages can narrow blood vessels and cause heart disease. Now, UConn Health researchers describe in Nature Cardiovascular Research how deleting a protein could prevent this and potentially prevent heart attacks and strokes in humans.

Macrophages are large white blood cells that cruise through our body as a kind of clean-up crew, clearing hazardous debris. But in people with atherosclerosis – fatty deposits and inflammation in their blood vessels – macrophages can cause trouble...

Sleep-modulating hormone hypocretin found to also control production of inflammatory cells. Getting enough sleep is key to good health, and studies have shown that insufficient sleep increases the risk of serious problems, including cardiovascular disease. Now Massachusetts General Hospital (MGH) investigators have discovered one way that sleep protects against the buildup of arterial plaques called atherosclerosis...

These images show a reduction in the number of macrophages infiltrating atherosclerotic plaques (in green) in animals treated with the IRE1 inhibitor. Credit: Image courtesy of University of California – Santa Barbara

Proteins begin life as long strings of amino acids that must fold into the 3D shape prescribed for their biological function. When proteins don’t fold as expected the cells activate stress responses meant to mitigate the problem. But severe or prolonged stress produces an acute response: Cell death is triggered to protect the organism.

Sustained activation of one such reaction – the unfolded protein response, or UPR – has been implicated in a number of diseases...