Autophagy could be used to Unfur Arteries

In a new study published in the journal Cell Metabolism, research led by the University Of Ottawa Heart Institute (UOHI) in Canada reveals that an ancient cellular pathway called autophagy mobilizes and exports cholesterol. This process of “self-digestion” for eliminating dysfunctional molecules from cells might enable the identification of new drug targets to “unfur arteries” or reverse atherosclerosis.

The study was led by investigator Dr Yves Marcel, Director of the HDL Biology Laboratory, UOHI, and colleagues from UOHI and Columbia University in New York, USA. The team found that cholesterol accumulated in the arterial walls is engulfed and digested by autophagy, a process initially developed in unicellular organisms.
In a statement, Marcel told the press: “The finding that autophagy also functions to digest and liberate cholesterol from cells and the fact that we know this pathway is regulated offers hope for the development of new drugs that could activate export of cholesterol the walls of arteries.”
Cholesterol being a significant molecule in mammals plays a vital role in hormone production and cell membrane development, and is transported across the body in the blood. However, it also tends to accumulate in the walls of the arteries, or “fur up,” causing atherosclerosis, thereby making the arteries narrower and narrower. This eventually results in blockages and decreased blood flow to the heart, often causing heart attacks and strokes.
Co-researcher Mireille Ouimet said, “There is an urgent need to understand how cholesterol accumulation in arteries can be reversed.”
The study findings reveal that autophagy itself is triggered by cholesterol accumulation. The process releases cholesterol from the arterial walls and transports it back to the liver to be metabolized and eliminated from the body.
Marcel speculates that the autophagy pathway might be disrupted in certain individuals with coronary artery disease (CAD), causing cholesterol accumulation.
New drugs could possibly target the reactivation of this pathway.