Mast cells, peptides and cardioprotection - An unlikely marriage?

S.K. Walsh, K.A. Kane, C.L. Wainwright

Research output: Contribution to journalArticle

8 Citations (Scopus)

Abstract

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. 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. 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.
LanguageEnglish
Pages73-84
Number of pages11
JournalAutonomic and Autacoid Pharmacology
Volume29
Issue number3
DOIs
Publication statusPublished - 2009

Fingerprint

Marriage
Mast Cells
Cell Degranulation
Peptides
Myocardial Ischemia
Ischemia
Relaxin
Adrenomedullin
Aptitude
Wounds and Injuries
Atrial Natriuretic Factor
Cardiovascular System

Keywords

  • myocardial ischaemia
  • cardioprotection
  • mast cells
  • endothelin
  • adrenomedullin
  • relaxin
  • atrial natriuretic peptide

Cite this

Walsh, S.K. ; Kane, K.A. ; Wainwright, C.L. / Mast cells, peptides and cardioprotection - An unlikely marriage?. In: Autonomic and Autacoid Pharmacology. 2009 ; Vol. 29, No. 3. pp. 73-84.
@article{217b1af188d54d90b66be693360dbbac,
title = "Mast cells, peptides and cardioprotection - An unlikely marriage?",
abstract = "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. 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. 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.",
keywords = "myocardial ischaemia, cardioprotection, mast cells, endothelin, adrenomedullin, relaxin, atrial natriuretic peptide",
author = "S.K. Walsh and K.A. Kane and C.L. Wainwright",
year = "2009",
doi = "10.1111/j.1474-8673.2009.00436.x",
language = "English",
volume = "29",
pages = "73--84",
journal = "Autonomic and Autacoid Pharmacology",
issn = "1474-8665",
number = "3",

}

Mast cells, peptides and cardioprotection - An unlikely marriage? / Walsh, S.K.; Kane, K.A.; Wainwright, C.L.

In: Autonomic and Autacoid Pharmacology, Vol. 29, No. 3, 2009, p. 73-84.

Research output: Contribution to journalArticle

TY - JOUR

T1 - Mast cells, peptides and cardioprotection - An unlikely marriage?

AU - Walsh, S.K.

AU - Kane, K.A.

AU - Wainwright, C.L.

PY - 2009

Y1 - 2009

N2 - 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. 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. 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.

AB - 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. 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. 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.

KW - myocardial ischaemia

KW - cardioprotection

KW - mast cells

KW - endothelin

KW - adrenomedullin

KW - relaxin

KW - atrial natriuretic peptide

UR - http://dx.doi.org/10.1111/j.1474-8673.2009.00436.x

U2 - 10.1111/j.1474-8673.2009.00436.x

DO - 10.1111/j.1474-8673.2009.00436.x

M3 - Article

VL - 29

SP - 73

EP - 84

JO - Autonomic and Autacoid Pharmacology

T2 - Autonomic and Autacoid Pharmacology

JF - Autonomic and Autacoid Pharmacology

SN - 1474-8665

IS - 3

ER -