Cardioprotective potential of annexin-A1 mimetics in myocardial infarction

Qin, C, Yang, Y, May, L, Gao, X, Stewart, A, Tu, Y, Woodman, O and Ritchie, R 2015, 'Cardioprotective potential of annexin-A1 mimetics in myocardial infarction', Pharmacology and Therapeutics, vol. 148, pp. 47-65.


Document type: Journal Article
Collection: Journal Articles

Title Cardioprotective potential of annexin-A1 mimetics in myocardial infarction
Author(s) Qin, C
Yang, Y
May, L
Gao, X
Stewart, A
Tu, Y
Woodman, O
Ritchie, R
Year 2015
Journal name Pharmacology and Therapeutics
Volume number 148
Start page 47
End page 65
Total pages 19
Publisher Elsevier Inc.
Abstract Myocardial infarction (MI) and its resultant heart failure remains a major cause of death in the world. The current treatments for patients with MI are revascularization with thrombolytic agents or interventional procedures. These treatments have focused on restoring blood flow to the ischemic tissue to prevent tissue necrosis and preserve organ function. The restoration of blood flow after a period of ischemia, however, may elicit further myocardial damage, called reperfusion injury. Pharmacological interventions, such as antioxidant and Ca2+ channel blockers, have shown premises in experimental settings; however, clinical studies have shown limited success. Thus, there is a need for the development of novel therapies to treat reperfusion injury. The therapeutic potential of glucocorticoid-regulated anti-inflammatory mediator annexin-A1 (ANX-A1) has recently been recognized in a range of systemic inflammatory disorders. ANX-A1 binds to and activates the family of formyl peptide receptors (G protein-coupled receptor family) to inhibit neutrophil activation, migration and infiltration. Until recently, studies on the cardioprotective actions of ANX-A1 and its peptide mimetics (Ac2-26, CGEN-855A) have largely focused on its anti-inflammatory effects as a mechanism of preserving myocardial viability following I-R injury. Our laboratory provided the first evidence of the direct protective action of ANX-A1 on myocardium, independent of inflammatory cells in vitro. We now review the potential for ANX-A1 based therapeutics to be seen as a "triple shield" therapy against myocardial I-R injury, limiting neutrophil infiltration and preserving both cardiomyocyte viability and contractile function. This novel therapy may thus represent a valuable clinical approach to improve outcome after MI.
Subject Pharmacology and Pharmaceutical Sciences not elsewhere classified
Keyword(s) Ac2-26
Cardiomyopathy
Cardioprotection
Formyl peptide receptors
Inflammation
Ischemia-reperfusion
DOI - identifier 10.1016/j.pharmthera.2014.11.012
Copyright notice © 2014 Elsevier Inc
ISSN 0163-7258
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