In the late 1960s, three Weizmann Institute of Science researchers developed several protein-like molecules, called copolymers, that they believed would produce a disease similar to multiple sclerosis in laboratory animals. The scientists—Prof. Michael Sela, Prof.
Ruth Arnon and Dr. Dvora Teitelbaum—were surprised to discover that, instead of causing the disease, the copolymers cured it; one of these molecules became the widely-used drug Copaxone. More than half a century later, in a new study being published today in Nature Cardiovascular Research , a research team from Weizmann's Molecular Cell Biology Department, headed by Prof.
Eldad Tzahor and Dr. Rachel Sarig, reveals that Copaxone might also facilitate recovery from a heart attack. Heart attacks happen when the supply of blood to part of the heart muscle is cut off.
Unless this supply is renewed quickly, the heart muscle cells start to die. Unlike skeletal muscle and other tissues that can recover from injury unscarred, heart muscle cells do not divide and do not replace dead cells with a new muscle. Instead, the heart's fibroblasts (that is, fiber cells) divide rapidly in the damaged area and create a network of protein fibers that replace the damaged cells with scar tissue.
This tissue ensures the integrity of the heart but reduces its ability to contract and pump blood. In the long term, therefore, a heart attack increases the chances of heart failure, a chronic condition in which the heart is incapable of meeti.