title: The Role of Redox Dysregulation in the Inflammatory Response to Acute Myocardial Ischaemia-reperfusion Injury - Adding Fuel to the Fire.
abstract: BACKGROUND
  The inflammatory response to acute myocardial ischaemia/ reperfusion injury (IRI) plays a critical role in determining myocardial infarct (MI) size, and subsequent post-MI left ventricular (LV) remodelling, making it a potential therapeutic target for improving clinical outcomes in patients presenting with an acute myocardial infarction (AMI). Recent experimental studies using advanced imaging and molecular techniques, have yielded new insights into the mechanisms through which reactive oxygen species (ROS) contribute to the inflammatory response induced by acute myocardial IRI - "adding fuel to the fire". The infiltration of inflammatory cells into the MI zone, leads to elevated myocardial concentrations of ROS, cytokine release, and activation of apoptotic and necrotic death pathways. Anti-oxidant and anti-inflammatory therapies have failed to protect the heart against acute myocardial IRI. This may be, in part, due to a lack of understanding of the time course, nature and mechanisms of the inflammation and redox dysregulation, which occur in the setting of acute myocardial IRI.
  
  
  CONCLUSIONS
  In this article, we examine the inflammatory response and redox dysregulation induced by acute myocardial IRI, and highlight potential therapeutic options for targeting redox dysregulation, in order to attenuate the detrimental effects of the inflammatory response following an AMI, so as to reduce MI size and prevent heart failure.
authors.affiliation: National Heart Research Institute Singapore, National Heart Centre Singapore, Singapore.|Cardiovascular and Metabolic Disorder Programme, Duke-NUS Medical School, Singapore.|Department of Cardiovascular Biomedicine, National Institute of Cardiology I. Ch, Mexico, Mexico City, Mexico.
authors.forename: Sauri
authors.initials: S
authors.lastname: Hernandez-Resendiz
authors.affiliation: Department of Physiology, Faculty of Medical Science, Naresuan University, Phitsanulok, Thailand.
authors.forename: Kroekkiat
authors.initials: K
authors.lastname: Chinda
authors.affiliation: National Heart Research Institute Singapore, National Heart Centre Singapore, Singapore.|Cardiovascular and Metabolic Disorder Programme, Duke-NUS Medical School, Singapore.
authors.forename: Sang-Bing
authors.initials: SB
authors.lastname: Ong
authors.affiliation: National Heart Research Institute Singapore, National Heart Centre Singapore, Singapore.|Cardiovascular and Metabolic Disorder Programme, Duke-NUS Medical School, Singapore.|Institute of Biochemistry, Medical School, Justus-Liebig-University, Giessen, Germany.
authors.forename: Hector
authors.initials: H
authors.lastname: Cabrera-Fuentes
authors.affiliation: Department of Cardiovascular Biomedicine, National Institute of Cardiology I. Ch, Mexico, Mexico City, Mexico.
authors.forename: Cecilia
authors.initials: C
authors.lastname: Zazueta
authors.affiliation: National Heart Research Institute Singapore, National Heart Centre Singapore, Singapore.|Cardiovascular and Metabolic Disorder Programme, Duke-NUS Medical School, Singapore.|Yong Loo Lin School of Medicine, National University Singapore, Singapore.|The Hatter Cardiovascular Institute, University College London, United Kingdom.|The National Institute of Health Research, University College London Hospitals, Biomedical Research Centre, London, United Kingdom.|Barts Heart Centre, St Bartholomew's Hospital, London, United Kingdom.
authors.forename: Derek J
authors.initials: DJ
authors.lastname: Hausenloy
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000627:therapeutic use; D006321:Heart / Q000503:physiopathology; D006801:Humans; D007249:Inflammation / Q000378:metabolism* / Q000503:physiopathology; D009203:Myocardial Infarction / Q000503:physiopathology; D015428:Myocardial Reperfusion Injury / Q000188:drug therapy / Q000378:metabolism* / Q000503:physiopathology; D009206:Myocardium / Q000378:metabolism*; D017382:Reactive Oxygen Species / Q000378:metabolism*
chemical_list: D000975:Antioxidants; D017382:Reactive Oxygen Species
keywords: Myocardial ischaemia/reperfusion injury; inflammation; neutrophils; oxidative stress; reactive oxygen species; redox dysregulation.