Fig. 1 | Cellular & Molecular Immunology

Fig. 1

From: Regulation of CD8+ T cells by lipid metabolism in cancer progression

Fig. 1

Lipid metabolism in cells. This figure illustrates the pathways of lipid metabolism in cells. Fatty acids (FAs) enter the cell through lipid translocases such as CD36, FABPs, and FATPs or via passive diffusion. Low-density lipoprotein (LDL) enters the cell through low-density lipoprotein receptors (LDLRs). Inside the cell, FAs are esterified to acyl-CoAs by ACSL enzymes for metabolism. Acyl-CoAs destined for catabolism are transported into mitochondria through CPTs to undergo fatty acid oxidation (FAO). Acetyl-CoA produced from FAO enters the TCA cycle, with electrons from NADH and FADH2 used in oxidative phosphorylation (OXPHOS) for ATP generation and oxygen respiration. Citrate from the TCA cycle can exit the mitochondria and be converted into acetyl-CoA by ACLY, initiating de novo fatty acid synthesis. Acetyl-CoA can be used by HMGCR for cholesterol synthesis or by FASN, along with malonyl-CoA, to produce palmitate, which is then activated to palmitoyl-CoA. Activated palmitate can be desaturated by SCDs to create monounsaturated and polyunsaturated fatty acids (MUFAs and PUFAs) and elongated by ELOVLs. Fatty acyl-CoAs combine with glycerol to form monoacylglycerols (MAGs), diacylglycerols (DAGs), and finally triacylglycerols (TAGs) via DGAT. TAGs are stored in lipid droplets, and lipases release FAs from TAGs, DAGs, and MAGs through hydrolysis. The figure also highlights the main transcriptional programs for lipid catabolism (PPARs) and anabolism (SREBPs)

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