Myocardial Infraction or without using the fancy medical term, simply, heart attack is a condition caused by limited blood supply to the heart muscles which results in the death of the tissues, eventually causing the patient to succumb to the condition.
In a more detailed sense, as we age, the blood vessel’s smooth inner walls that supply the blood to heart become damaged and narrow due to the buildup of fatty materials, called plaque. And when this area breaks, blood cells and other parts of the blood stick to the damaged area and form blood clots. This in turn leads to a blockage in the organ that reduces the flow of blood causing heart attacks.
Monocytes, as part of their job profile to respond to inflammation, generally flock to cholesterol deposits, where they either become inflammatory forces (M1)—contributing to plaque buildup—or they become healing cells (M2).
Now, a new study by a group at the NYU Langone Medical Center have found a way to engineer Monocytes to help heal these arterial vessel instead of causing a buildup of plaque ultimately resulting in heart attacks. They have now confirmed that timing is extremely vital in bringing about the crucial switch to
M2 versus M1 macrophage. When monocytes arrive in regressing plaques, they become M2 macrophages, controlling inflammation and preventing dangerous plaque ruptures and have identified other, for instance the Ly6Chigh monocytes that change to take over an inflammatory role.Therefore the scientists are working on identifying these particular signals that tell those monocytes to become M2 macrophages.
“A race is underway to develop treatments that enhance the decision of human monocytes to become M2 macrophages in cases where the disease has not yet caused clot formation, at which point it becomes irreversible,” said Edward Fisher, the lead scientist.
Fisher’s team as of now have some candidates such as immune signaling proteins interleukin-4 and interleukin-13 in mind for further analysis, and are also taking an alternative route to examine HDL and its interaction with nanoparticles; since HDL, aka the “good cholesterol” is known to remove LDL from plaques and shuttle it to the liver, where it is destroyed.
