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This may also explain the loss of contractile function during metabolic inhibition (Figures 1, 2), where the Kir6.2/SUR2A channels, the well-established canonical cardiac K ATP channel subunits, would also be open (Brennan et al., 2024
CpG oligonucleotide, a TLR9 agonist, enhanced the antitumor potential of macrophages by increasing FAO and shunting of acetyl-CoA toward lipid substances synthesis, which needed the involvement of CPT1A and ATP citrate lyase (Liu et al., 2019)
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