Transactivation of the epidermal growth factor receptor in responses to myocardial stress and cardioprotection

Reichelt, Melissa E., O'Brien, Shannon, Thomas, Walter G. and Headrick, John P. (2017) Transactivation of the epidermal growth factor receptor in responses to myocardial stress and cardioprotection. International Journal of Biochemistry and Cell Biology, 83 97-110. doi:10.1016/j.biocel.2016.12.014


Author Reichelt, Melissa E.
O'Brien, Shannon
Thomas, Walter G.
Headrick, John P.
Title Transactivation of the epidermal growth factor receptor in responses to myocardial stress and cardioprotection
Journal name International Journal of Biochemistry and Cell Biology   Check publisher's open access policy
ISSN 1878-5875
1357-2725
Publication date 2017-02-01
Year available 2016
Sub-type Critical review of research, literature review, critical commentary
DOI 10.1016/j.biocel.2016.12.014
Open Access Status Not yet assessed
Volume 83
Start page 97
End page 110
Total pages 14
Place of publication Kidlington, Oxford, United Kingdom
Publisher Pergamon Press
Language eng
Abstract The epidermal growth factor receptor (EGFR) family comprises the ErbB1 (EGFR) and ErbB4 receptors as well as the ‘co-receptors’ ErbB2 (which does not bind EGF ligands) and ErbB3 (which lack tyrosine kinase activity). This family of receptors is essential for cardiac development, myocardial, renal and vascular function, and cardiac responses to physiological and pathological perturbations. The EGFR appears critical in protecting cardiac cells from injury, while considerable attention has focussed on neuregulin/ErbB4 signalling in potentially ameliorating cardiomyopathy/heart failure. Indeed, the EGFRs provide a signalling nexus, upon which multiple cardioprotective stimuli appear to converge, including ischaemic preconditioning and various G protein-coupled receptors (opioid, muscarinic, adenosine, adrenergic, bradykinin, sphingosine 1-phosphate). These stimuli engage the EGFR axis (in a process referred to as transactivation) in differing ways, involving both G protein-dependent and -independent mechanisms, to promote myocardial cell survival during and following ischaemia/infarction. Elucidating the molecular processes that underpin EGFR transactivation and mediate cardiac protection will advance our understanding of the intrinsic capacity of the heart to withstand pathological insult. It should also reveal new approaches to facilitate cardioprotective therapy to limit damage during and following myocardial ischaemia/infarction, which despite intense investigation remains an unrealised, yet highly desirable, clinical goal. This review focuses on the cardiovascular functions of the EGFR, its role in cardioprotection, and the potential influences of common disease states on this signalling.
Keyword Cardioprotection
EGFR
ErbB
G protein-coupled receptors
Ischaemia-reperfusion
Preconditioning
Transactivation
Q-Index Code C1
Q-Index Status Provisional Code
Institutional Status UQ

Document type: Journal Article
Sub-type: Critical review of research, literature review, critical commentary
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School of Biomedical Sciences Publications
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