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. 2022 Dec 6;13(12):2301. doi: 10.3390/genes13122301

Figure 1.

Figure 1

EC FA metabolism. Fatty acids (FAs) are transported in the form of triglyceride (TG)-rich lipoproteins, which are released by lipoprotein lipase (LPL) and GPIHBP1 in the luminal side of ECs. Free FAs are transported across EC membranes by fatty acid transporter protein 3 and 4 (FATP3/4) and CD36. Intracellular FAs transportation is mediated by FABP3 and FABP4. Intracellular FAs could be synthesized by FA synthase (FASN) from Malonyl-CoA and affect mTORC1 activity for angiogenesis. DAGTs and ATGL are key enzymes regulating lipid droplet (LD) storage and lipolysis. FAs are transported into mitochondria via CPT1 for FA oxidation (FAO). Quiescent ECs utilize FAO to maintain redox homeostasis. FAO is required for the generation of dNTPs for EC spouting and angiogenesis. In certain conditions such as glucose depletion, FAO produces ATP in ECs. FAO also produces acetyl-CoA for epigenetic regulation, inhibiting EndoMT. The efflux of FAs to the perivascular cells could be mediated by FABP4/5 and FATP3/4. Many key endothelial signaling including VEGF, NOTCH, and PPAR γ control EC FA transport via regulating FATPs, FABPs, and CD36.