Induction of Autophagy Slows High Fat Diet Induced Atherosclerosis in Mice

Atherosclerosis is the name given to the growth of fatty lesions in blood vessel walls, narrowing and weakening blood vessels, and eventually rupturing to cause a heart attack or stroke. This is the primary cause of human mortality. Many approaches have been demonstrated to slow the progression of atherosclerosis in the most commonly used mouse models, in which atherosclerosis is rapidly induced by a combination of high fat diet and the disabling of genes, such as APOE and LDLR, that are important to maintain normal blood cholesterol levels and cholesterol transport. Very few approaches have been shown to produce a reduction in the size of atherosclerotic lesions once they are established, however. In today's open access paper, researchers demonstrate that a small molecule capable of provoking increased autophagy in a number of cell types relevant to atherosclerosis can meaningfully slow development of lesions in APOE-knockout mice. This is reasonable. Dysfunction in both (a) the endothelial cells lining blood vessels and (b) the macrophages responsible for clearing cholesterol from blood vessel walls is important in atherosclerosis. Increased operation of autophagy tends to help cells resist stresses that would otherwise disable them, kill them, or change their behavior for the worse, such as by inducing a senescent state. It should be expected to adjust the tipping points for formation and growth of atherosclerotic lesions. It most likely won't do anything to reverse...
Source: Fight Aging! - Category: Research Authors: Tags: Medicine, Biotech, Research Source Type: blogs