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. Author manuscript; available in PMC: 2021 Dec 9.
Published in final edited form as: Cell Rep. 2021 Oct 5;37(1):109767. doi: 10.1016/j.celrep.2021.109767

Figure 7. Working model: PHD2/3, CPT1B, and VDAC1 may work together in cardiomyocytes under normoxic condition.

Figure 7.

PHD2/3 catalyze prolyl-4-hydroxylation on CPT1B P295 residue, which promotes CPT1B/VDAC1 complex formation and facilitates LFCA mitochondrial uptake. Hypoxia inhibits PHD2/3 enzymatic activity, resulting in the disruption of CPT1B/VDAC1 complex and inhibition of LCFA mitochondrial uptake and metabolism.