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Article

Ectonucleotidase CD39-driven control of postinfarction myocardial repair and rupture.

JCI insight - 12 Jan 2017

Sutton Nadia R, Hayasaki Takanori, Hyman Matthew C, Anyanwu Anuli C, Liao Hui, Petrovic-Djergovic Danica, Badri Linda, Baek Amy E, Walker Natalie, Fukase Keigo, Kanthi Yogendra, Visovatti Scott H, Horste Ellen L, Ray Jessica J, Goonewardena Sascha N, Pinsky David J

Abstract excerpt

Mechanical complications of myocardial infarction (MI) are often fatal. Little is known about endogenous factors that predispose to myocardial rupture after MI. Ectonucleoside triphosphate diphosphohydrolase (CD39) could be a critical mediator of propensity to myocardial rupture after MI due to its role in modulating inflammation and thrombosis. Using a model of permanent coronary artery ligation, rupture was...

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Share to Adenosine Triphosphatases
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Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

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Identifiers

PMID: 28097233
DOI: 10.1172/jci.insight.89504
PMCID: PMC5213916

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PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 5 Sept 2026. Manifest publication-graph-cohort-2026-09-05.1.

Source receipt: pubmed, retrieved 5 Sept 2026.

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