• Such a series of destructive events has been implicated in diseases such as rheumatoid arthritis, myocardial infarction/reperfusion injury, atherogenesis, asthma, cystic fibrosis, emphysema, and vasculitis. (lu.se)
  • The pathophysiological nature of MIRI is the short-term disturbance of myocardial energy and metabolism caused by reflow after ischemia and hypoxia in the coronary artery and the dynamic changes in apoptosis and the prosurvival signaling pathways in response to related injury factors. (hindawi.com)
  • Myocardial I/R injury may induce cell apoptosis and autophagy by activating oxidative stress and upregulating inflammatory mediators, ultimately resulting in irreversible fibrotic damage ( 3 ). (spandidos-publications.com)
  • In conclusion, myocardial damage in MI is mainly due to ischemic necrosis and inflammatory mechanisms while apoptosis is the main mechanism of cell death in IR in addition to limited ischemic necrosis. (aku.edu)
  • Upregulation of Fas expression in myocardial ischemia-reperfusion can induce cardiomyocyte apoptosis, and atorvastatin can significantly inhibit cardiomyocyte apoptosis by inhibiting Fas expression. (ac.ir)
  • Apoptosis of the cardiomyocytes has been demonstrated in animal models with coronary artery occlusion [ 1 ], and experimental evidence suggests that myocardial cells are able to undergo apoptosis during ischemia followed by reperfusion [ 2 ]. (ac.ir)
  • Both ischemic and reperfused rat myocardium can undergo apoptotic cell death, however the myocardium, which is subjected to ischemia followed by reperfusion, undergoes accelerated apoptosis [ 3 ]. (ac.ir)
  • Ticagrelor, but not clopidogrel, increased myocardial adenosine levels, increased phosphorylation of Akt, endothelial NO synthase, and extracellular-signal-regulated kinase 1/2 4 hours after reperfusion and decreased apoptosis. (utmb.edu)
  • In rats and pigs, BSPC@HM NCs remarkably downregulates Sav1 in IR-injured myocardium, promotes myocardium regeneration, suppresses myocardial apoptosis, and recovers cardiac functions. (scimage.cn)
  • The most effective early treatment for reducing AMI injury and limiting the infarcted myocardium is timely coronary revascularization using thrombolytic therapy or primary percutaneous coronary intervention (PPCI) [ 2 - 4 ]. (hindawi.com)
  • This coupled comorbidity of pathological ischemia and therapeutic reinjury of infarcted myocardium, namely, myocardial ischemia-reperfusion injury (MIRI), is particularly refractory to treatment [ 4 , 5 ]. (hindawi.com)
  • During injury stimulation, the major effects on the cardiac function may be those involving mitochondria-dominated events along with potential nucleus-governed genetic/epigenetic alternations within the cardiomyocytes as well as the macrophage-led inflammation and T-cell-led immune responses underlying the myocardium-vessel interactive cascade. (hindawi.com)
  • GRh2 reduced the area of myocardial infarction and the histological changes in the myocardium and improved cardiac functions. (spandidos-publications.com)
  • Reperfusion has the potential to salvage ischemic myocardium but paradoxically can cause injury, a phenomenon called as 'reperfusion injury' (IR). (aku.edu)
  • These pleiotropic effects thus have a major role in protecting the myocardium against ischemic injury. (ac.ir)
  • The Canadian Cardiovascular Society (CCS) has developed a four-stage classification of acute atherothrombotic myocardial infarction (MI) based on the severity of the injury to the myocardium. (medscape.com)
  • Because the major source of CK-MB is myocardium, an elevated CK-MB level reflects myocardial injury, including acute myocardial infarction, myocarditis, cardiac trauma, cardiac surgery, and endomyocardial biopsy. (medscape.com)
  • Myocardial infarction (MI) denotes the death of cardiac myocytes due to extended ischemia. (aku.edu)
  • It has been shown that the Fas pathway is functional in cardiac myocytes and plays a critical role in myocardial death due to ischemia-reperfusion in vivo [ 4 ]. (ac.ir)
  • In lpr mice, a naturally occurring mutant deficient in Fas, there is marked reduction in infarct size and abundance of apoptotic cardiac myocytes following ischemia and reperfusion that also signifies the importance of Fas pathway in ischemia-reperfusion injury [ 5 ]. (ac.ir)
  • Hypercholesterolemia causes endothelial and myocardial dysfunction, as well as aggravates ischemia/reperfusion (I/R)-induced myocardial injury. (nih.gov)
  • The role of cardiac proteasome dysfunction during I/R and the perspective to diminish I/R injury by manipulating proteasome function remain unclear. (elsevierpure.com)
  • The study aims to examine the effects of coenzyme Q10, (a bioenergetic antioxidant), on the indexes of left ventricular remodeling, oxidative damage, and angiotensin-converting enzyme (ACE) level after acute myocardial infarction (AMI) with left ventricular dysfunction. (mdpi.com)
  • Meng X, Zhang L, Han B and Zhang Z: PHLDA3 inhibition protects against myocardial ischemia/reperfusion injury by alleviating oxidative stress and inflammatory response via the Akt/Nrf2 axis. (spandidos-publications.com)
  • The findings of the present study indicated that inhibition of miR‑132 may ameliorate myocardial I/R injury by inhibiting oxidative stress and pyroptosis through activation of PGC‑1α/Nrf2 signalling by targeting SIRT1. (spandidos-publications.com)
  • Rationale: Both cardiomyocyte-restricted proteasome functional enhancement and pharmacological proteasome inhibition (PSMI) were shown to attenuate myocardial ischemia/reperfusion (I/R) injury. (elsevierpure.com)
  • It has been reported that SIRT1/peroxisome proliferator-activated receptor gamma coactivator (PGC)-1α/nuclear factor erythroid-2-related factor 2 (Nrf2) signalling can mediate oxidative stress, which plays an important role in myocardial I/R injury ( 14 , 15 ). (spandidos-publications.com)
  • While effective early reperfusion of the criminal coronary artery after a confirmed AMI is the typical treatment at present, collateral myocardial ischemia-reperfusion injury (MIRI) and pertinent cardioprotection are still challenging to address and have inadequately understood mechanisms. (hindawi.com)
  • Our results indicate that estrogen plays a cardioprotective role in global myocardial ischemia-reperfusion injury in female rats. (illinois.edu)
  • Atorvastatin has been shown to be cardioprotective in ischemia-reperfusion (I/R) injury. (ac.ir)
  • Remote ischaemic preconditioning (RIPC) has been shown to reduce perioperative myocardial injury (PMI) in patients having CABG even when cold blood cardioplegia or intermittent cross clamp fibrillation is used as cardioprotective measures. (druglib.com)
  • Oral dosing of rats with SCN-, before acute ischemia-reperfusion injury (30 min occlusion, 24 h or 4 week recovery), significantly reduced the infarct size as a percentage of the total reperfused area (54% versus 74%), and increased the salvageable area (46% versus 26%) as determined by MRI imaging. (ku.dk)
  • Objective To determine the impact of time-of-day onset of ST segment elevation myocardial infarction (STEMI) on infarct size. (bmj.com)
  • It was also reported that miR-132 was upregulated in simulated ischaemic injury in cultured hippocampal neurons ( 12 ). (spandidos-publications.com)
  • Relationships between structure and effects of ACE inhibitors: comparative effects in myocardial ischaemic/reperfusion injury. (cmich.edu)
  • Dive into the research topics of 'Relationships between structure and effects of ACE inhibitors: comparative effects in myocardial ischaemic/reperfusion injury. (cmich.edu)
  • The purpose of this study is to determine whether Glyceryl Trinitrate (GTN) reduces injury to the heart during heart-lung bypass surgery in combination with the newer technique of remote ischaemic preconditioning (RIPC). (druglib.com)
  • Supplementation also decreased antibody recognition of HOCl-damaged myocardial proteins. (ku.dk)
  • Cardiac markers or cardiac enzymes are proteins that leak out of injured myocardial cells through their damaged cell membranes into the bloodstream. (wikipedia.org)
  • In conclusion, the present study confirmed that GRh2 could reduce oxidative stress and inflammation in cardiomyocytes after reperfusion, and its mechanism of action may be related to its regulation of the Nrf2/HO‑1/NLRP3 signalling pathway. (spandidos-publications.com)
  • Sun W, Wang Z, Sun M, Huang W and Wang Y and Wang Y: Aloin antagonizes stimulated ischemia/reperfusion-induced damage and inflammatory response in cardiomyocytes by activating the Nrf2/HO-1 defense pathway. (spandidos-publications.com)
  • Among clinical emergency events, ST-segment elevation (STE) or the non-STE electrocardiogram diagnosis of acute myocardial infarction (AMI) is particularly common worldwide, with a staggering number of annual first episodes as well as recurrent ones [ 1 ]. (hindawi.com)
  • Patients' data for the study were obtained from the EARLY-MYO-CMR (Early Assessment of Myocardial Tissue Characteristics by CMR in STEMI) registry, which was a prospective, multicenter registry of patients with ST-segment elevation myocardial infarction (STEMI) who underwent cardiac magnetic resonance (CMR) imaging after reperfusion therapy. (physiciansweekly.com)
  • citation needed] The 12 lead ECG is used to classify patients into one of three groups: those with ST segment elevation or new bundle branch block (suspicious for acute injury and a possible candidate for acute reperfusion therapy with thrombolytics or primary PCI), those with ST segment depression or T wave inversion (suspicious for ischemia), and those with a so-called non-diagnostic or normal ECG. (wikipedia.org)
  • In patients with ST-segment elevation myocardial infarction (STEMI), ischemic postconditioning (iPOST) have shown ambiguous results in minimizing reperfusion injury. (lu.se)
  • We investigated the effects of estrogen on global myocardial ischemia-reperfusion injury in rats that were ovariectomized (Ovx), sham-operated, or ovariectomized and then given 17β-estradiol (E 2 β) supplementation (Ovx+E 2 β). (illinois.edu)
  • Thirty Wistar rats were selected and divided into three groups (n = 10): acute ischemia-reperfusion (I/R) group, acute ischemia-reperfusion and treated with atorvastatin group and sham-operated group. (ac.ir)
  • Approach and Results - Rats underwent 30-minute ischemia per 24-hour reperfusion. (utmb.edu)
  • Despite substantial declines in mortality following myocardial infarction (MI), subsequent left ventricular remodeling (LVRm) remains a significant long-term complication. (researchgate.net)
  • Imaging tests such as stress radionuclide myocardial perfusion imaging or stress echocardiography can confirm a diagnosis when a person's history, physical exam, ECG and cardiac biomarkers suggest the likelihood of a problem. (wikipedia.org)
  • Numerous apoptotic cardiomyocytes were found in ischemic fields in ischemia-reperfusion groups and werent observed in the sham-operated group. (ac.ir)
  • It was shown that functional Fas system contributes to apoptotic myocardial cell death in response to ischemia/reperfusion injury [ 4 , 5 ]. (ac.ir)
  • Worldwide morbidity and mortality from acute myocardial infarction (AMI) and related heart failure remain high. (hindawi.com)
  • Mechanism investigations revealed a unique nuclear receptor subfamily 1 group D member 1/cardiotrophin-like cytokine factor 1 axis in the heart, which was critical in mediating the negative effects of shift work on myocardial damage. (physiciansweekly.com)
  • Interleukin-36 (IL-36), a newly discovered proinflammatory member of the IL-1 superfamily, may mediate this injury, but its role in the injured heart is currently not known. (jci.org)
  • An intravital model for imaging the adult and aged IR-injured beating heart in real time in vivo was used to demonstrate heightened basal and injury-induced neutrophil recruitment, and poorer blood flow, in the aged coronary microcirculation when compared with adult hearts. (jci.org)
  • A diagnosis of myocardial infarction is created by integrating the history of the presenting illness and physical examination with electrocardiogram findings and cardiac markers (blood tests for heart muscle cell damage). (wikipedia.org)
  • In experimental groups A (n = 10) and B (n = 10), metabolic control of autoregulation was assessed by plots of myocardial oxygen consumption versus coronary flow generated by incremental increases in heart rate. (elsevierpure.com)
  • In addition, it has been shown that atorvastatin can protect the isolated mouse heart against reperfusion-induced injury [ 6 ]. (ac.ir)
  • We reported that there is infarct expansion after reperfusion, so once you open up the vessel, the heart attack actually gets larger. (medscape.com)
  • Commercial kits were used to measure the levels of serum myocardial enzymes and inflammatory factors. (spandidos-publications.com)
  • Apparent histologic injury and elevated levels of serum myocardial enzymes and inflammatory factors were observed in the myocardial I/R model. (spandidos-publications.com)
  • and the increased morning levels of serum cortisol and plasma catecholamines leading to sympathetic overactivity, thereby resulting in increased myocardial demand. (medscape.com)
  • Neonatal rat cardiomyocytes were also used to evaluate the protective effect of GRh2 on hypoxia/reoxygenation (H/R)‑induced myocardial injury in vitro. (spandidos-publications.com)
  • 1. MicroRNA-503 (miR-503) exacerbates myocardial ischemia/reperfusion (I/R) injury by inhibiting prosurvival signaling pathways, including PI3K/Akt and STAT3. (fullpicture.app)
  • The GRh2 pre‑treatment reduced the I/R‑ or H/R‑induced release of myocardial enzymes and the production of IL‑1β, IL‑18 and TNF‑α. (spandidos-publications.com)
  • Until the 1980s, the enzymes SGOT and LDH were used to assess cardiac injury. (wikipedia.org)
  • Therefore, our aim was to develop a medium throughput comorbidity cell-based test system of myocardial I/R injury, hypercholesterolemia and hyperglycemia that mimics comorbidity conditions. (nih.gov)
  • The objectives of this study were to 1) determine the extent to which ascorbate or catechin alone at levels which could be in blood after dietary supplementation, can protect myocardial tissue in the reperfusion phase of I/R injury, and 2) evaluate the possible cooperative or synergistic protective effect of ascorbate and catechin when given together. (usask.ca)
  • The myocardial I/R model was established using C57BL/J6 mice. (spandidos-publications.com)
  • Methods and Results: Myocardial I/R were modeled by ligation (30 minutes) and subsequent release of the left anterior descending artery in mice overexpressing GFPdgn, a validated surrogate proteasome substrate. (elsevierpure.com)
  • Beneficial effects of IL-37 after spinal cord injury in mice. (nature.com)
  • However, while myocardial reperfusion is well established, the process itself can trigger myocardial reperfusion injury by causing further cardiomyocyte death through multiple pathophysiological mechanisms [ 3 - 5 ]. (hindawi.com)
  • Conceptual diagram of the development and unknown mechanisms of myocardial ischemia-reperfusion injury. (hindawi.com)
  • However, despite numerous studies on myocardial I/R injury, deeper insight into the underlying mechanisms of myocardial I/R injury is needed. (spandidos-publications.com)
  • However, few studies have focused on the role of miR-132 in myocardial I/R injury and the underlying mechanisms. (spandidos-publications.com)
  • The needleless approach provides millions of patients with potential myocardial ischemic diseases a minimum risk solution for examining their coronary circulation without the potential harm from the standard clinical exams. (cedars-sinai.edu)
  • 2 ] hypothesised that the phosphatidylcholines are prime oxidising targets in the asthmatic airway based on their relative abundance, and that oxidised phosphatidylcholines (OxPC) are mechanistic effectors of oxidised stress in asthma, suggested by prior research demonstrating the ability of OxPC to perpetuate inflammation in ageing-related diseases, and their known causal role in both acute lung injury and acute respiratory distress syndrome [ 3 - 5 ]. (ersjournals.com)
  • Increased CK is predominantly used to diagnose neuromuscular diseases and acute myocardial infarction. (medscape.com)
  • CK can also be elevated in the absence of neuromuscular diseases or cardiac injury, such as after strenuous exercise, intramuscular injection, and with renal disease. (medscape.com)
  • this may be an important mechanism of decreased coronary perfusion and subsequent myocardial injury during reflow. (elsevierpure.com)
  • abstract = "To determine the mechanism(s) responsible for decreased coronary flow after global cardiac ischemia and reperfusion, we studied 40 isolated rabbit hearts before and after 30 minutes of normothermic ischemic arrest and reperfusion. (elsevierpure.com)
  • 3. Agomir-503 treatment worsens hypoxia/reoxygenation-induced injuries, while antagomir-503 treatment attenuates them and increases phosphorylation of Stat3 (Y705) and Akt (T450). (fullpicture.app)
  • miR‑132 was significantly upregulated and SIRT1 was markedly downregulated in I/R myocardial tissues. (spandidos-publications.com)
  • Fas expression was significantly higher in the ischemia-reperfusion group as compared to sham-operated group, but was decreased significantly in atorvastatin treated group as compared with I/R group. (ac.ir)
  • At 24 hours of reperfusion, myocardial proteasome activities were significantly lower whereas total ubiquitin conjugates and GFPdgn protein levels were markedly higher in all regions of the I/R hearts than the sham controls, indicative of proteasome functional insufficiency. (elsevierpure.com)