Targeted deletion of A3 adenosine receptors improves tolerance to ischemia-reperfusion injury in mouse myocardium

A3 adenosine receptors (A3ARs) have been implicated in regulating mast cell funcjtion and in cardioprotection during ischemia-reperfusion injury. The physiological role of A3ARs is unclear due to the lack of widely available selective antagonists.

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Bibliographic Details
Published inAmerican journal of physiology. Heart and circulatory physiology Vol. 50; no. 4; pp. H1751 - H1758
Main Authors CERNIWAY, Rachael J, ZEQUAN YANG, JACOBSON, Marlene A, LINDEN, Joel, MATHERNE, G. Paul
Format Journal Article
LanguageEnglish
Published Bethesda, MD American Physiological Society 01.10.2001
Subjects
Biological and medical sciences
Cardiology
Cardiology. Vascular system
Circulatory system
Coronary heart disease
Heart
Heart attacks
Medical sciences
Rodents
Heart
Rodentia
Site directed mutagenesis
Transgenic animal
Cardiovascular disease
Inflammation
Coronary heart disease
Myocardial disease
A3 adenosine receptor
Vascular disease
Vertebrata
Mammalia
Reperfusion
Ischemia
Mouse
Myocardium
Circulatory system
Lesion
Preconditioning
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Summary:A3 adenosine receptors (A3ARs) have been implicated in regulating mast cell funcjtion and in cardioprotection during ischemia-reperfusion injury. The physiological role of A3ARs is unclear due to the lack of widely available selective antagonists.
ISSN:0363-6135
1522-1539