Innate Immune Inflammatory Response in the Acutely Ischemic Myocardium
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.
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.
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