Innate Immune Inflammatory Response in the Acutely Ischemic Myocardium

ISSN: 1875-6638 (Online)
ISSN: 1573-4064 (Print)


Volume 10, 8 Issues, 2014


Download PDF Flyer




Medicinal Chemistry

Aims & ScopeAbstracted/Indexed in


Submit Abstracts Online Submit Manuscripts Online

Editor-in-Chief:
Atta-ur-Rahman, FRS
Honorary Life Fellow
Kings College
University of Cambridge
Cambridge
UK
Email: mc@benthamscience.org

View Full Editorial Board

Subscribe Purchase Articles Order Reprints

Current: 1.387
5 - Year: 1.379

Innate Immune Inflammatory Response in the Acutely Ischemic Myocardium

Author(s): Spyridon Deftereos, Christos Angelidis, Georgios Bouras, Konstantinos Raisakis, Ulrich Gerckens, Michael W. Cleman and Georgios Giannopoulos

Affiliation: Department of Cardiology, Athens General Hospital “G. Gennimatas” Mesogeion 154, 11527, Athens, Greece.

Abstract

The “holy grail” of modern interventional cardiology is the salvage of viable myocardial tissue in the distribution of an acutely occluded coronary artery. Thrombolysis and percutaneous coronary interventions, provided they can be delivered on time, can interrupt the occlusion and save tissue. At the same time restoring the patency of the coronary vessels and providing the ischemic myocardium with blood can cause additional tissue damage. A key element of ischemic and reperfusion injury and major determinant of the evolution of damage in the injured myocardium is the inflammatory response. The innate immune system initiates and directs this response which is a prerequisite for subsequent healing. The complement cascade is set in motion following the release of subcellular membrane constituents. Endogenous ‘danger’ signals known as danger-associated molecular patterns (DAMPs) released from ischemic and dying cells alert the innate immune system and activate several signal transduction pathways through interactions with the highly conserved Toll like receptors (TLRs). Reactive oxygen species (ROS) generation directly induces pro-inflammatory cascades and triggers formation of the inflammasome. The challenge lies into designing strategies that specifically block the inflammatory cascades responsible for tissue damage without affecting those concerned with tissue healing.

Keywords: Complement, danger associated molecular patterns, innate immune system, inflammation, inflammasome, ischemia/ reperfusion, reactive oxygen species, toll like receptors.

Purchase Online Rights and Permissions

  
  



Article Details

Volume: 10
Issue Number: 7
First Page: 653
Last Page: 662
Page Count: 10
DOI: 10.2174/1573406410666140806103651
Advertisement

Related Journals




Webmaster Contact: urooj@benthamscience.org Copyright © 2014 Bentham Science