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dc.contributor.authorWalsh, S K
dc.contributor.authorKane, K A
dc.contributor.authorWainwright, C L
dc.date.accessioned2012-01-31T16:42:19Z
dc.date.available2012-01-31T16:42:19Z
dc.date.issued2012-01-31T16:42:19Z
dc.identifier.citationAuton Autacoid Pharmacol. 2009 Jul;29(3):73-84.en_GB
dc.identifier.issn1474-8673 (Electronic)en_GB
dc.identifier.issn1474-8665 (Linking)en_GB
dc.identifier.pmid19566747en_GB
dc.identifier.doi10.1111/j.1474-8673.2009.00436.xen_GB
dc.identifier.urihttp://hdl.handle.net/10147/206240
dc.description.abstract1 Mast cells have classically been regarded as the 'bad guys' in the setting of acute myocardial ischaemia, where their released contents are believed to contribute both to tissue injury and electrical disturbances resulting from ischaemia. Recent evidence suggests, however, that if mast cell degranulation occurs in advance of ischaemia onset, this may be cardioprotective by virtue of the depletion of mast cell contents that can no longer act as instruments of injury when the tissue becomes ischaemic. 2 Many peptides, such as ET-1, adrenomedullin, relaxin and atrial natriuretic peptide, have been demonstrated to be cardioprotective when given prior to the onset of myocardial ischaemia, although their physiological functions are varied and the mechanisms of their cardioprotective actions appear to be diverse and often ill defined. However, one common denominator that is emerging is the ability of these peptides to modulate mast cell degranulation, raising the possibility that peptide-induced mast cell degranulation or stabilization may hold the key to a common mechanism of their cardioprotection. 3 The aim of this review was to consolidate the evidence implying that mast cell degranulation could play both a detrimental and protective role in myocardial ischaemia, depending upon when it occurs, and that this may underlie the cardioprotective effects of a range of diverse peptides that exerts physiological effects within the cardiovascular system.
dc.language.isoengen_GB
dc.subject.meshAnimalsen_GB
dc.subject.mesh*Cardiotonic Agentsen_GB
dc.subject.meshCell Degranulationen_GB
dc.subject.meshHeart Diseases/pathology/*physiopathologyen_GB
dc.subject.meshHumansen_GB
dc.subject.meshMast Cells/*physiologyen_GB
dc.subject.meshMyocardial Ischemia/pathology/physiopathologyen_GB
dc.subject.meshMyocardium/pathologyen_GB
dc.subject.meshNeuropeptides/*pharmacology/*physiologyen_GB
dc.titleMast cells, peptides and cardioprotection - an unlikely marriage?en_GB
dc.contributor.departmentAnu Research Centre, Department of Obstetrics & Gynaecology, University College, Cork, Cork University Maternity Hospital, Cork, Ireland.en_GB
dc.identifier.journalAutonomic & autacoid pharmacologyen_GB
dc.description.provinceMunster
html.description.abstract1 Mast cells have classically been regarded as the 'bad guys' in the setting of acute myocardial ischaemia, where their released contents are believed to contribute both to tissue injury and electrical disturbances resulting from ischaemia. Recent evidence suggests, however, that if mast cell degranulation occurs in advance of ischaemia onset, this may be cardioprotective by virtue of the depletion of mast cell contents that can no longer act as instruments of injury when the tissue becomes ischaemic. 2 Many peptides, such as ET-1, adrenomedullin, relaxin and atrial natriuretic peptide, have been demonstrated to be cardioprotective when given prior to the onset of myocardial ischaemia, although their physiological functions are varied and the mechanisms of their cardioprotective actions appear to be diverse and often ill defined. However, one common denominator that is emerging is the ability of these peptides to modulate mast cell degranulation, raising the possibility that peptide-induced mast cell degranulation or stabilization may hold the key to a common mechanism of their cardioprotection. 3 The aim of this review was to consolidate the evidence implying that mast cell degranulation could play both a detrimental and protective role in myocardial ischaemia, depending upon when it occurs, and that this may underlie the cardioprotective effects of a range of diverse peptides that exerts physiological effects within the cardiovascular system.


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