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Some variants have clear structural explanations for their loss-of-function, for example, variants can disrupt binding of carnitine (R471C/H/P), affect the Na + -binding site (N32S), disrupt the TM2-TM11 H-bonding network (S467C) or perturb gating residues conserved in OCTs/OATs (R169Q/P/W)

Metabolic homeostasis and abnormalities have spurred major interest in the field of AF at present, with a focus on lipids, the predominant energy substrates (70%) of heart

However, intramitochondrial L-carnitine can export both short-chain and medium-chain acyl-CoA out of the mitochondria, that otherwise could lead to the production of free radicals which can destabilize the cell membrane

A proportion of infants and children with sepsis progress to cardiac failure as part of multiple system organ failure (hepatic, renal, cardiac, pulmonary) [100]