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.
Medicinal Chemistry
Title:Innate Immune Inflammatory Response in the Acutely Ischemic Myocardium
Volume: 10 Issue: 7
Author(s): Spyridon Deftereos, Christos Angelidis, Georgios Bouras, Konstantinos Raisakis, Ulrich Gerckens, Michael W. Cleman and Georgios Giannopoulos
Affiliation:
Keywords: Complement, danger associated molecular patterns, innate immune system, inflammation, inflammasome, ischemia/ reperfusion, reactive oxygen species, toll like receptors.
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.
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Cite this article as:
Deftereos Spyridon, Angelidis Christos, Bouras Georgios, Raisakis Konstantinos, Gerckens Ulrich, Cleman W. Michael and Giannopoulos Georgios, Innate Immune Inflammatory Response in the Acutely Ischemic Myocardium, Medicinal Chemistry 2014; 10 (7) . https://dx.doi.org/10.2174/1573406410666140806103651
DOI https://dx.doi.org/10.2174/1573406410666140806103651 |
Print ISSN 1573-4064 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-6638 |
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