Genetic modulation of adenosine receptor function and adenosine handling in murine hearts: Insights and issues

Kevin J. Ashton, Jason N. Peart, R. Ray Morrison, G. Paul Matherne, Michael R. Blackburn, John P. Headrick

Research output: Contribution to journalReview articleResearchpeer-review

12 Citations (Scopus)

Abstract

The adenosine receptor system has been attributed with a broad range of both physiological and so-called 'retaliatory' functions in the heart and vessels. Despite many years of research, the precise roles of adenosine within the cardiovascular system continue to be debated, and new functions are continually emerging. Adenosine acts via 4 known G-protein-coupled receptor (GPCR) sub-types: A1, A2A, A2B, and A3 adenosine receptors (ARs). In addition to roles in cardiovascular control, these receptors may represent therapeutic targets, having been attributed with roles in modifying cell death and injury, inflammatory processes, and cardiac and vascular remodeling during/after ischemic or hypoxic insult. A number of models have been developed in which AR sub-types and adenosine handling enzymes have been genetically deleted or transgenically overexpressed in an attempt to more equivocally identify the regulatory functions of these proteins, to identify their potential value as therapeutic targets, and to uncover new regulatory functions of this receptor family. Findings generally support current dogma regarding cardioprotection via A1 and A3ARs, and coronary vasoregulation via A2AR sub-types. However, some outcomes are both novel and controversial. This review outlines AR-modified murine models currently under study from the perspective of cardiovascular phenotype.

Original languageEnglish
Pages (from-to)693-705
Number of pages13
JournalJournal of Molecular and Cellular Cardiology
Volume42
Issue number4
DOIs
Publication statusPublished - Apr 2007
Externally publishedYes

Fingerprint

Purinergic P1 Receptors
Adenosine
Adenosine A2B Receptors
Adenosine A3 Receptors
Adenosine A2A Receptors
Adenosine A1 Receptors
Cardiovascular System
Cell Death
Phenotype
Wounds and Injuries
Enzymes
Therapeutics
Research
Proteins

Cite this

Ashton, Kevin J. ; Peart, Jason N. ; Morrison, R. Ray ; Matherne, G. Paul ; Blackburn, Michael R. ; Headrick, John P. / Genetic modulation of adenosine receptor function and adenosine handling in murine hearts : Insights and issues. In: Journal of Molecular and Cellular Cardiology. 2007 ; Vol. 42, No. 4. pp. 693-705.
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abstract = "The adenosine receptor system has been attributed with a broad range of both physiological and so-called 'retaliatory' functions in the heart and vessels. Despite many years of research, the precise roles of adenosine within the cardiovascular system continue to be debated, and new functions are continually emerging. Adenosine acts via 4 known G-protein-coupled receptor (GPCR) sub-types: A1, A2A, A2B, and A3 adenosine receptors (ARs). In addition to roles in cardiovascular control, these receptors may represent therapeutic targets, having been attributed with roles in modifying cell death and injury, inflammatory processes, and cardiac and vascular remodeling during/after ischemic or hypoxic insult. A number of models have been developed in which AR sub-types and adenosine handling enzymes have been genetically deleted or transgenically overexpressed in an attempt to more equivocally identify the regulatory functions of these proteins, to identify their potential value as therapeutic targets, and to uncover new regulatory functions of this receptor family. Findings generally support current dogma regarding cardioprotection via A1 and A3ARs, and coronary vasoregulation via A2AR sub-types. However, some outcomes are both novel and controversial. This review outlines AR-modified murine models currently under study from the perspective of cardiovascular phenotype.",
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Genetic modulation of adenosine receptor function and adenosine handling in murine hearts : Insights and issues. / Ashton, Kevin J.; Peart, Jason N.; Morrison, R. Ray; Matherne, G. Paul; Blackburn, Michael R.; Headrick, John P.

In: Journal of Molecular and Cellular Cardiology, Vol. 42, No. 4, 04.2007, p. 693-705.

Research output: Contribution to journalReview articleResearchpeer-review

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