Myocardial Reperfusion Injury

By L. Becker. Journal of Thrombosis and Thrombolysis, 2004

2,012 citations recorded by the source corpus.

Subfields: Pathology and Forensic Medicine, Pharmacology

View Paper: https://www.semanticscholar.org/paper/0ae37139d05784c2c274bcc7c9445855b3138b48

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In Pathology and Forensic Medicine

In Pharmacology

Citations in the corpus

Report from a consensus conference on primary graft dysfunction after cardiac transplantation. (2014, neutral): “30 The combination of Ca 2 þ overload and high oxidant stress in an energy-depleted cardiac myocyte activates formation of the mitochondrial permeability transition pore (MPTP), a non-speci ﬁ c channel that forms in the mitochondrial membrane and allows pro-apoptotic factors, such as cytochrome C,…”
The pathophysiology of acute myocardial infarction and strategies of protection beyond reperfusion: a continual challenge. (2016, background): “and the coronary circulation and it contributes to final infarct size.(10,11) The prevention and treatment of lethal reperfusion injury”
A Unifying Mechanism for Mitochondrial Superoxide Production during Ischemia-Reperfusion Injury. (2016, background): “Deactive complex I exposes a critical cysteine residue (Cys39 in the ND3 subunit in mammals) that is occluded in active complex I (Chouchani et al., 2013; Galkin et al., 2008; Gorenkova et al., 2013; Zickermann et al., 2015) (Figure 3B).”
Cell Biology of Ischemia/Reperfusion Injury (2012, methodology): “…that is fueled by reintroduction of molecular oxygen when the blood flow is reestablished, (2) calcium overload, (3) opening of the MPT pore, (4) endothelial dysfunction, (5) appearance of a prothrombogenic phenotype, and (6) pronounced inflammatory responses (Yellon and Hausenloy, 2007) (Fig.”
Myocardial ischemia-reperfusion injury: a neglected therapeutic target. (2013, neutral): “The major contributory factors are discussed below and include oxidative stress, calcium overload, mitochondrial permeability transition pore (MPTP) opening, and hypercontracture (3).”
2011 ACCF/AHA Guideline for Coronary Artery Bypass Graft Surgery. A report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. Developed in collaboration with the American Association for Thoracic Surgery, Society of Cardiovascular Anesthesi (2011, neutral): “onlinejac Downloaded from ell death (205).”
Fourth Universal Definition of Myocardial Infarction (2018). (2018, neutral): “Mitochondrial abnormalities are observed as early as 10 min after coronary occlusion by electron microscopy and are progressive (17).”
Mitochondrial dysfunction: mechanisms and advances in therapy (2024, background): “221 Overexpression of the mitochondrial Na + /Ca 2 + exchanger (NCLX) could enhance Ca 2 + clearance, reduce permeability transition, and prevent myocardial cell necrosis and heart failure due to ischemia.”
Management of acute myocardial infarction in patients presenting with persistent ST-segment elevation: the Task Force on the Management of ST-Segment Elevation Acute Myocardial Infarction of the European Society of Cardiology. (2008, background): “99 No-reflow may occur as a consequence of downstream microvascular embolization of thrombotic or atheromatous (lipid-rich) debris, reperfusion injury, microvascular disruption, endothelial dysfunction, inflammation, and myocardial oedema.(100,101)”
The IL-33/ST2 pathway: therapeutic target and novel biomarker (2008, background): “More recent attempts to manipulate the inflammatory response to myocardial injury in humans have also been met with limited clinical success (reviewed in Ref”
Ferroptosis: a cell death connecting oxidative stress, inflammation and cardiovascular diseases (2021, background): “However, restoration of circulation is accompanied with inevitable cell death, oxidative stress damage, inflammation and programmed cell death, and eventually results in tissue injury such as myocardial infarction (MI) [80].”
Can Animal Models of Disease Reliably Inform Human Studies? (2010, background): “Differences between animal models and clinical trials similar to those mentioned above have been proposed as causes of the recurrent failure of a range of strategies to reduce lethal reperfusion injury in patients with acute myocardial infarction [6,7].”
Fourth Universal Definition of Myocardial Infarction (2018). (2018, neutral): “Mitochondrial abnormalities are observed as early as 10 min after coronary occlusion by electron microscopy and are progressive.(17) It can take hours before myocyte necrosis can be identified by postmortem examination in humans; this is in contrast to animal models, in which biochemical evidence of”
Mitochondrial dynamics in health and disease: mechanisms and potential targets (2023, background): “However, it is important to note that reperfusion itself can lead to cardiomyocyte death, which is known as myocardial reperfusion injury.(211) Currently, no effective treatments are available for this condition.”
Myocardial no-reflow in humans. (2009, background): “A massive infiltration of cornary microcirculation by neutrophils and platelets occurs at he time of reperfusion (19,22).”