Reversal of atherosclerosis is a much harder problem, and the work involving increased autophagy noted here is not a demonstration of reversal, but rather just another demonstration of slowed atherosclerosis. Small differences sustained over time add up. It is actually not that hard to significantly slow the growth of atherosclerotic plaque in mice, and many methods work well. The chronic inflammation and oxidative stress of age disrupts the ability of macrophages sufficiently to allow atherosclerotic plaques to form in the first place, but once formed the plaque is a hostile environment that overwhelms macrophages with excess cholesterol.Īnything that improves macrophage resilience can help. In atherosclerosis, fatty deposits build up in blood vessels as a result of macrophages becoming less capable of returning excess cholesterol to the blood stream. In today's research materials, the team involved in developing autophagy-upregulating small molecule therapies at Life Biosciences discuss evidence for chaperone-mediated autophagy to be relevant in atherosclerosis. Upregulation of autophagy for long periods of time is a feature of numerous interventions, such as calorie restriction and calorie restriction mimetics, that result in slowed aging. It appears to decline in quality with age, leading to downstream problems in cell and tissue function as worn and damaged component parts accumulate. Autophagy is quite clearly connected to tissue function and aging in a number of ways. These materials are delivered to a lysosome, a membrane packed with enzymes capable of dismantling near every macromolecule a cell will encounter, producing raw materials for reuse. Forms of autophagy function to remove unwanted, excess, or damaged structures and other molecules in the cell.
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