Endothelial Cell Senescence Accelerates Atherosclerosis

Atherosclerosis, a condition in which fatty lesions form to narrow, weaken, and distort blood vessel walls, might be primarily thought of as a condition of macrophage dysfunction. The innate immune cells called macrophages are responsible for clearing out unwanted lipids from blood vessel walls. Unfortunately, the growing prevalence of oxidized lipids and an inflammatory environment arising in later life causes macrophages to falter at this task. Macrophages become inflammatory rather than helpful in the lesion environment, then are overwhelmed and die, but are still attracted in ever greater numbers to swell the size of the lesion. Researchers have shown that some of these inflammatory and dysfunctional macrophages are senescent, and that removing them via the use of senolytic therapies helps to slow the progression of atherosclerosis in animal models. In today's open access paper, the role of senescent endothelial cells in blood vessel walls is considered. Senescent cells secrete inflammatory signals, so any population of senescent cells in the vicinity of an atherosclerotic lesion will make things worse by biasing macrophages towards adopting an inflammatory, unhelpful state, rather than working on repair of the lesion. Given that, it is unclear as to which of the populations of senescent cell types in and around atherosclerotic lesions are most influential on the progression of the condition and growth of lesions, as present senolytic treatments will destroy...
Source: Fight Aging! - Category: Research Authors: Tags: Medicine, Biotech, Research Source Type: blogs