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Editorial
. 2021 Jan 1;117(1):15-17.
doi: 10.1093/cvr/cvaa149.

Cyclophilin D palmitoylation and permeability transition: a new twist in the tale of myocardial ischaemia-reperfusion injury

Alice Main  1 , Olivia Robertson-Gray  1 , William Fuller  1
Affiliations
Editorial

Cyclophilin D palmitoylation and permeability transition: a new twist in the tale of myocardial ischaemia-reperfusion injury

Alice Main et al. Cardiovasc Res. .
No abstract available

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Figures

Figure 1
Figure 1
CypD C202 Modification in Cardiac Mitochondria. Amanakis et al. demonstrate that under basal conditions, the mitochondrial permeability transition pore (PTP) regulator cyclophillin-D (CypD) is reported to be both S-nitrosylated and S-palmitoylated at position cysteine 202 (C202). Under conditions of ischaemia, CypD S-palmitoylation and S-nitrosylation are reduced as C202 undergoes oxidation. This leads to greater association of CypD with the F1-ATPase subunit of the PTP and enhances pore opening and calcium efflux at reperfusion, thus leading to greater myocardial damage and increased infarct size. Mutation of C202 to a serine (S) results in no possible modification by S-nitrosylation, S-palmitoylation but also S-oxidation and transgenic mice have significantly reduced infarct size and enhanced functional recovery as a result.
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