Researchers from the Albert Einstein College of Medicine have recently discovered a possible way of preventing clogged arteries and, in turn, reducing the risks of strokes and heart attacks. The novel technique involves supercharging the body's natural cleaning process that slows down as a person ages.
Supercharging the Body's Cleaning Process
A vital part of the study is chaperone-mediated autophagy, wherein damaged or unneeded proteins are degraded. In doing so, CMA regulates numerous vital processes in the body, such as the circadian rhythms, cellular metabolism, and DNA repair, typically in response to cellular stress. On the other hand, the effectiveness of CMA slows down as a person ages, which results in the build-up of proteins that can contribute to some familiar age-related diseases, like Alzheimer's.
In the recent study published in the journal PNAS, titled "Protective role of chaperone-mediated autophagy against atherosclerosis," researchers were able to identify a novel problem that CMA helps protect against - atherosclerosis, otherwise, the build-up of plaque in the body's arteries known to lead to heart attacks and strokes. Experts found that CMA is activated in response to cellular stress of high-fat diets, which initially works to stall the accumulation of plaque, but over time loses out.
Dr. Ana Maria Cuervo, the lead author from the Department of Development and Molecular Biology at Albert Einstein College of Medicine, explains that the research demonstrates how CMA is needed to protect against atherosclerosis which is known to become more severe and progress when the body's CMA declines - something known to happen as people age. She adds that the study has also proven that increasing the activity of CMA can be an effective tool in curbing atherosclerosis and halting its progression.
Studying the Effects of Increased CMA Activity
Researchers examined the complex role of CMA in the conditions by initially feeding mice high-fat diets for a total of 12 weeks, monitoring the mice' CMA activity in two cell types that are known to malfunction in atherosclerosis. The CMA activity in mice increased during the early stages of the experiment in response to the sudden stress brought by the mice's unhealthy diet. Intriguingly, by the 12th week, there was almost zero CMA activity in the mice' cells, reports NewAtlas.
In other tests, the team repeated the experiment on mice models that have been engineered to lack CMA activity. After 12 weeks on the unhealthy high-fat diet, the mice developed plaques roughly 40% higher than the control mice of the same diet.
Although mice and human biology largely differ, researchers were able to find evidence linking CMA to atherosclerosis in humans. By analyzing the CMA activity in clogged arteries removed from 62 patients who had previously suffered strokes.
Cuervo explains that the patients observed with higher levels of CMA following the first stroke never had a second attack. In contrast, second strokes occurred in almost all patients with lower CMA activity. Data suggests that a person's CMA activity level can help predict the risks for a second stroke and help in guiding treatments for patients with lower CMA.
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