Lipid Metabolism

 Lipid metabolism is altered in cancer—tumor cells reactivate de novo lipid synthesis, ATP-citrate lyase is required for transformation in vitro, cholesterol synthesis in prostate cancer is increased, and fatty acid oxidation is an important source of energy for prostate cancer cells. Autophagy in the specific form of lipophagy is important for the degradation of lipid droplets in the adipose tissue and autophagy regulates lipid metabolism in hepatocytes as triglyceride hydrolysis.


Additionally, autophagy impacts lipid metabolism by altering the mitochondrial number. Atg7 deleted, p53 mutant cells in a KRAS-driven NSCLC model have intracellular lipid accumulation because of increased dysfunctional mitochondria that compromises fatty acid oxidation, suggesting that autophagy is crucial to maintain lipid metabolism in KRAS and p53 mutant cells. Lipid metabolism and the passage of low-density lipoproteins (LDL) out of the arterial lumen and into the arterial wall are the basis for the development of atherosclerosis. LDL particles accumulate in the vessel wall and initiate the formation of atherosclerotic plaque formation. Macrophages internalize LDL, become enlarged and full of lipids, and then transform into foam cells. Parts of the foam cell and dying macrophages accumulate in vessel walls, thereby participating in atherosclerotic plaque formation. Reduced levels of high-density lipoprotein (HDL) and cholesterol are known risk factors together with high levels of LDL. HDL is involved with the transport of excess cholesterol from macrophages and other cells, so it is vital for diminishing the accumulation of foam cells in atherosclerosis.

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