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. 2022 Jun 28;6(7):e740. doi: 10.1097/HS9.0000000000000740

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Copyright © 2022 the Author(s). Published by Wolters Kluwer Health, Inc. on behalf of the European Hematology Association.

This is an open access article distributed under the Creative Commons Attribution License 4.0 (CCBY), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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Figure 6. — Fatty acid oxidation sustains HSCs. FAO, a key catabolic pathway for energy production, fuels the TCA cycle rather than glycolysis. Long-chain fatty acids are first activated in the cytosol in fatty acyl-CoA, and then transported by the carnitine shuttle system, which is composed by CPT1, CACT, and CPT2, into the mitochondria. Here, β-oxidation through multi-step reactions generates acetyl-CoA, which fuels the TCA cycle. Mitochondrial FAO is critical for HSC maintenance: PML regulates the PPARδ, through the transcription factor PGC1α. PPARδ is a regulator of FAO, and its deletion results in loss of HSC reconstitution potential. Template created with BioRender.com. CACT = carnitine-acylcarnitine translocase; CPT1 = carnitine palmitoyltransferase 1; CPT2 = carnitine palmitoyltransferase 2; FAO = fatty acid oxidation; HSC = hematopoietic stem cell; PGC1α = PPARg coactivator-1α; PML = promyelocytic leukemia; PPARδ = peroxisome-proliferator activated receptor delta; TCA = tricarboxylic acid.