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
From https://jamesjohnson10.blogspot.com/2019/11/trib1-regulates-uptake-of-oxidized.html
from
https://jamesjohnson10.wordpress.com/2019/11/09/trib1-regulates-uptake-of-oxidized-lipids-into-macrophages-and-thus-drives-atherosclerosis/
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