TRIB1 Regulates Uptake of Oxidized Lipids into Macrophages, and thus Drives Atherosclerosis

Atherosclerosis is a condition of dysfunctional macrophages. Macrophages are responsible for clearing out lipids that end up in blood vessel walls, ingesting these misplaced lipid molecules and handing them off to HDL particles to be carried to the liver for excretion. This works just fine in youth, in an environment of low oxidative stress and few oxidized lipids. Aging brings chronic inflammation, oxidative stress, and oxidized lipids, however. Macrophages cannot process oxidized lipids all that well, and so become pathological, turning into inflammatory foam cells packed with lipids, and unable to do more than send signals for help. The plaques that form to narrow and weaken blood vessels in atherosclerosis might start out as lipid deposits, but become macrophage graveyards as they grow, as ever more macrophages arrive to try and fail to clear the damage. A number of new approaches to atherosclerosis based on interfering in this process are under development. My company, Repair Biotechnologies, works on a way to allow macrophages to break down oxidized cholesterol in situ. Underdog Pharmaceuticals works on sequestration of the worst oxidized lipid, 7-ketocholesterol. And so forth. The work here, in which researchers identify the gene TRIB1 as a regulator of macrophage uptake of oxidized lipids, offers a new avenue of attack. The evidence presented is fairly compelling for some form of inhibition of TRIB1 to be the basis for a therapy. If this could be done for an ex...
Source: Fight Aging! - Category: Research Authors: Tags: Medicine, Biotech, Research Source Type: blogs