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Journal of Cellular and Molecular Medicine logoLink to Journal of Cellular and Molecular Medicine
. 2021 Jan 17;25(2):1325. doi: 10.1111/jcmm.16095

CORRIGENDUM

PMCID: PMC7812283

In Zuurbier et al, 1 the published article contains errors in Table 1. The correct table is shown below. The authors confirm all results, conclusions of this article remain unchanged.

TABLE 1.

FAO inhibitors for IRI

Compound Mechanism/target Activity in models of MI Model Ref
sulfo‐N‐succinimidyl oleate (SSO) Inhibition of sarcolemmal FAT/CD36 Prevented cardiac dysfunction after ischaemia Isolated diabetic and control male Wistar rat harts [161]

CBM‐301940

CBM‐300864

Inhibition of malonyl CoA decarboxylase Improved cardiac function during and after ischaemia

Isolated rat hearts

Pigs in vivo

[162, 163]
Methyl‐GBB decreased accumulation of long‐chain acylcarnitines Decreased MI size, improved survival

ligation of LAD, rats

Isolated perfused rat hearts

[164]
Trimetazidine

long‐chain 3‐ketoacyl‐CoA thiolase inhibitor

AMPK and ERK signalling pathways

Reduced MI size and oxidative stress in vivo regional ischaemia and reperfusion, mice [165]
carvedilol adrenergic receptor blocker; modulator of cardiac AMPK signalling pathway MI size reduction, improved cardiac functions ligation of LAD, mice [166]

Abbreviations: LAD, left anterior descending coronary artery; MI, myocardial infarction.

REFERENCE

  • 1. Zuurbier CJ, Bertrand L, Beauloye CR, et al. Cardiac metabolism as a driver and therapeutic target of myocardial infarction. J Cell Mol Med. 2020;24:5937‐5954. 10.1111/jcmm.15180 [DOI] [PMC free article] [PubMed] [Google Scholar]

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