The Scientific World Journal, 2012 Background. Revascularization of infarcted myocardium results in release of inflammatory cytokines mediating myocardial reperfusion injury and heart failure. Blockage of inflammatory pathways dampens myocardial injury and reduces infarct size.
Christina Grothusen +6 more
doaj +1 more source
Confocal laser scanning microscope, raman microscopy and western blotting to evaluate inflammatory response after myocardial infarction [PDF]
, 2015 Cardiac muscle necrosis is associated with inflammatory cascade that clears the infarct from dead cells and matrix debris, and then replaces the damaged tissue with scar, through three overlapping phases: the inflammatory phase, the proliferative phase
Cantatore, S +6 more
core +1 more source
Platelets, diabetes and myocardial ischemia/reperfusion injury
Cardiovascular Diabetology, 2017 Mechanisms underlying the pathogenesis of ischemia/reperfusion injury are particularly complex, multifactorial and highly interconnected. A complex and entangled interaction is also emerging between platelet function, antiplatelet drugs, coronary diseases and ischemia/reperfusion injury, especially in diabetic conditions.
RUSSO, Isabella +6 more
openaire +3 more sources
The role of neutrophils in myocardial ischemia–reperfusion injury [PDF]
Cardiovascular Research, 1999 Reperfusion of ischemic myocardium is necessary to salvage tissue from eventual death. However, reperfusion after even brief periods of ischemia is associated with pathologic changes that represent either an acceleration of processes initiated during ischemia per se, or new pathophysiological changes that were initiated after reperfusion.
J E, Jordan +2 more
openaire +2 more sources
Cytoprotective Activated Protein C Averts Nlrp3 Inflammasome–Induced Ischemia-Reperfusion Injury Via Mtorc1 Inhibition [PDF]
, 2017 Cytoprotection by activated protein C (aPC) after ischemia-reperfusion injury (IRI) is associated with apoptosis inhibition. However, IRI is hallmarked by inflammation, and hence, cell-death forms disjunct from immunologically silent apoptosis are, in ...
Al-Dabet, Moh\u27d Mohanad +16 more
core +2 more sources
Decreased myocardial injury and improved contractility after administration of a peptide derived against the alpha-interacting domain of the L-type calcium channel. [PDF]
, 2014 BackgroundMyocardial infarction remains the leading cause of morbidity and mortality associated with coronary artery disease. The L-type calcium channel (IC a-L) is critical to excitation and contraction.
Hool, Livia C +3 more
core +1 more source
Estrogen Protects the Female Heart from Ischemia/Reperfusion Injury through Manganese Superoxide Dismutase Phosphorylation by Mitochondrial p38β at Threonine 79 and Serine 106. [PDF]
, 2016 A collective body of evidence indicates that estrogen protects the heart from myocardial ischemia/reperfusion (I/R) injury, but the underlying mechanism remains incompletely understood. We have previously delineated a novel mechanism of how 17β-estradiol
Kim, Jin Kyung, Liu, Han, Luo, Tao
core +1 more source
Stem Cell Research & Therapy, 2021 Background Ischemia-reperfusion injury (IRI) is an important factor limiting the success of cardiac reperfusion therapy. Curcumin has a significant cardioprotective effect against IRI, can inhibit ventricular remodeling induced by pressure load or MI ...
Chi-Lin Liao +5 more
doaj +1 more source
Bench-to-bedside review: Erythropoietin and its derivatives as therapies in critical care [PDF]
, 2012 Author can archive publisher's pdf. Free via Creative Commons: CC-BENCHTOBEDSIDE-2.0.
Nandra, KK, Patel, NSA, Thiemermann, C
core +1 more source
Nitric oxide in myocardial ischemia/reperfusion injury [PDF]
Cardiovascular Research, 2004 Administration of nitric oxide (NO), NO donors or drugs that enhance NO release (statins, calcium antagonists, ACE-inhibitors, dexamethasone) prior to ischemia protects the myocardium against ischemia/reperfusion injury. While this exogenous administration of NO prior to ischemia can initiate a preconditioning-like phenomenon, endogenous NO-synthase ...
Rainer, Schulz +2 more
openaire +2 more sources