Publication: Myeloperoxidase: a potential therapeutic target for coronary artery disease
Issued Date
2020-01-01
Resource Type
ISSN
17447631
14728222
14728222
Other identifier(s)
2-s2.0-85084421308
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Mahidol University
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SCOPUS
Bibliographic Citation
Expert Opinion on Therapeutic Targets. (2020)
Suggested Citation
Thanat Chaikijurajai, W. H.Wilson Tang Myeloperoxidase: a potential therapeutic target for coronary artery disease. Expert Opinion on Therapeutic Targets. (2020). doi:10.1080/14728222.2020.1762177 Retrieved from: https://repository.li.mahidol.ac.th/handle/20.500.14594/56136
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Title
Myeloperoxidase: a potential therapeutic target for coronary artery disease
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Abstract
© 2020, © 2020 Informa UK Limited, trading as Taylor & Francis Group. Introduction: Coronary artery disease (CAD) poses significant morbidity and mortality globally. Despite significant advances in treatment interventions, residual cardiovascular risks remain unchecked. Recent clinical trials have shed light on the potential therapeutic benefits of targeting anti-inflammatory pathways. Myeloperoxidase (MPO) plays an important role in atherosclerotic plaque formation and destabilization of the fibrous cap; both increase the risk of atherosclerotic cardiovascular disease and especially CAD. Areas covered: This article examines the role of MPO in the pathogenesis of atherosclerotic CAD and the mechanistic data from several key therapeutic drug targets. There have been numerous interesting studies on prototype compounds that directly or indirectly attenuate the enzymatic activities of MPO, and subsequently exhibit atheroprotective effects; these include aminobenzoic acid hydrazide, ferulic acid derivative (INV-315), thiouracil derivatives (PF-1355 and PF-06282999), 2-thioxanthines derivative (AZM198), triazolopyrimidines, acetaminophen, N-acetyl lysyltyrosylcysteine (KYC), flavonoids, and alternative substrates such as thiocyanate and nitroxide radical. Expert opinion: Future investigations must determine if the cardiovascular benefits of direct systemic inhibition of MPO outweigh the risk of immune dysfunction, which may be less likely to arise with alternative substrates or MPO inhibitors that selectively attenuate atherogenic effects of MPO.