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Editorial
. 2021 Jun 24;137(25):3465-3467.
doi: 10.1182/blood.2021011475.

Break the lifeline of AML cells

Yoko Tabe  1   2 , Marina Konopleva  1
Affiliations
Editorial

Break the lifeline of AML cells

Yoko Tabe et al. Blood. .
No abstract available

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Figures

None
Mitochondrial FAO pathway and therapeutic targets. The scavenger receptor CD36 facilitates the uptake of long-chain FAs into the cytoplasm of AML cells. Inside the cells, FAs are first transported by FA-binding proteins (FABPs) and other transport proteins, followed by activation in a 2-step reaction: forming acyl-CoA in the cytoplasm and then FAO, forming acetyl-CoA inside mitochondria. CPT-1 conjugates FAs to carnitine, a prerequisite for mitochondrial translocation of FAs from the cytoplasm. In mitochondria, VLCAD, an intramitochondrial FAO enzyme, starts to catalyze the dehydrogenation reaction of long-chain FAs as the first intramitochondrial step of FAO. FAO generates ATP and provides acetyl-CoA to the tricarboxylic acid (TCA) cycle.
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References

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