• 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)
  • However, whether GRh2 has a protective effect on ischaemia/reperfusion (I/R) in the myocardium has yet to be elucidated. (spandidos-publications.com)
  • During open heart surgery, the myocardium suffers from ischemia-reperfusion injury (IR) despite perioperative cardioprotection. (oroboros.at)
  • Slagsvold KH, Rognmo O, Hoydal M, Wisloeff U, Wahba A (2014) Remote ischemic preconditioning preserves mitochondrial function and influences myocardial microrna expression in atrial myocardium during coronary bypass surgery. (oroboros.at)
  • 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)
  • These pleiotropic effects thus have a major role in protecting the myocardium against ischemic injury. (ac.ir)
  • Restoration of blood flow rescues myocardium but also causes ischemia-reperfusion injury. (sinica.edu.tw)
  • Protection of the ischemic myocardium is known to occur as a result of ischemic preconditioning (PC), in which repetitive brief periods of ischemia protect the heart from a subsequent prolong ischemic insult. (eurekaselect.com)
  • In the ischemic myocardium, an increase in glucose uptake and subsequent ATP generated through glycolysis helps to sustain myocardial electric and mechanical performance, maintains cellular ultrastructure, promotes myocardial recovery. (biomedcentral.com)
  • The injured myocardium develops an evolving dependence on glucose as its preferred metabolic substrate while development of myocardial insulin resistance is associated with the progression of heart failure and increased incidence as well as severity of the damaged hearts. (biomedcentral.com)
  • Stunned myocardium is myocardium that suffers transient reversible myocardial contractile dysfunction that is caused by acute ischemia during which the blood supply is almost completely restored by reperfusion, with no metabolic deterioration. (medscape.com)
  • The term hibernating myocardium is also used to indicate chronic myocardial contractile dysfunction due to ischemia, in which there is reduced coronary blood flow at rest and increased myocardial demand results in impaired contractility. (medscape.com)
  • Rahimtoola suggested that hibernating myocardium is characterized by a state of persistently impaired myocardial and LV function at rest due to reduced coronary blood flow that can be partially or completely restored to normal by improving blood flow or by reducing oxygen demand (see the image below). (medscape.com)
  • Clinically, discerning the etiology of depressed myocardial contractile function is difficult, whether due to stunned myocardium, silent ischemia, or hibernating myocardium. (medscape.com)
  • Expression of LTBP2 was elevated and specifically localized in the fibrotic regions of the myocardium after injury in mice and in human heart failure, suggesting that it may be a potential therapeutic target. (libsyn.com)
  • 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)
  • 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)
  • Compared to rats, AGS display robust myocardial ischemic tolerance following DHCA (both reduced myocardial necrosis and apoptosis). (duke.edu)
  • All of these factors are known to result in myocardial apoptosis(5) and the acceleration of allograft rejection or chronic allograft dysfunction. (researchsquare.com)
  • D. odorifera may be a potential candidate drug for treating myocardial ischemic injury. (wjtcm.net)
  • Our current projects are focused on: 1) Rescue and Role of Complex I in Myocardial Ischemic Injury 2) Subcellular Regulation of Autophagy 3) Mitochondria and Stem Cells in Anthracycline-Induced Heart Failure 4) Development of Small-Molecular Cardioprotective Agents for Treatment of Reperfusion Injury and 5) Microbial Basis of Cardiovascular Disease. (pewtrusts.org)
  • These findings were further confirmed when HIF-1 stabilization in the rat and murine heart resulted in smaller myocardial infarct sizes (both in vivo and ex vivo), decreased mitochondrial oxidative stress, and inhibited MPTP opening following IRI, effects which were also found to be dependent on HKII. (ox.ac.uk)
  • 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)
  • Short series of repetitive cycles of brief reperfusion and re-occlusion of the coronary artery applied at the onset of reperfusion, reduce the infarct size and coronary artery endothelial dysfunction. (eurekaselect.com)
  • Methods and results: Hearts from PKN1 knockout (KO) or wild type (WT) littermate control mice were perfused in Langendorff mode and subjected to global ischaemia and reperfusion (I/R). Myocardial infarct size was doubled in PKN1 KO hearts compared to WT hearts. (figshare.com)
  • Conclusion: Loss of PKN1 in vivo significantly reduces endogenous cardioprotection and increases myocardial infarct size following I/R injury. (figshare.com)
  • We hypothesize that one bout of exercise one day prior to open heart surgery is sufficient to induce cardioprotection and preserve mitochondrial function. (oroboros.at)
  • Pharmacological inhibition of extracellular signal-regulated kinase activation in the PVA abolishes neuropathic pain-induced cardioprotection, whereas activation of PVA neurons pharmacologically, or optogenetic stimulation, is sufficient to induce cardioprotection. (sinica.edu.tw)
  • It was shown that functional Fas system contributes to apoptotic myocardial cell death in response to ischemia/reperfusion injury [ 4 , 5 ]. (ac.ir)
  • The possible underlying mechanism of the cardioprotective effect of T. terrestris could be due to restoration of endogenous myocardial antioxidant status or free radical scavenging activity along with correction of the altered hemodynamic parameters and preservation of histoarchitectural and ultrastructural alterations. (scialert.net)
  • Our laboratory combines comparative biology approaches in multiple organisms with translational functional genomics to study the mechanisms underlying perioperative myocardial injury, with a particular emphasis on endogenous cardioprotective responses involving attenuation of nuclear factor-kappa B regulated inflammatory signaling and changes in myocardial fuel utilization. (duke.edu)
  • Another endogenous form of cardioprotection, similar to PC but applicable at the time of reperfusion, termed postconditioning (PostC), has been recently described. (eurekaselect.com)
  • The aim was to determine its role in endogenous cardioprotection. (figshare.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)
  • 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)
  • It is important to understand how these mechanisms are dynamically regulated by pivotal molecular targets and potentially reversed in the context of cardioprotection [ 6 ]. (hindawi.com)
  • Conceptual diagram of the development and unknown mechanisms of myocardial ischemia-reperfusion injury. (hindawi.com)
  • The present study aimed to investigate the roles of miR‑132 in myocardial ischaemia/reperfusion (I/R) injury and the underlying mechanisms. (spandidos-publications.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 key mechanisms underlying myocardial I/R injury include increased intracellular calcium concentration, sudden generation of reactive oxygen species (ROS) and inflammatory cytokines, adenosine triphosphate (ATP) depletion, and development of metabolic acidosis. (researchsquare.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)
  • METHODS AND RESULTS: Stabilization of myocardial HIF-1 was achieved by pharmacological inhibition of prolyl hydroxylase (PHD) domain-containing enzyme using GSK360A or using cardiac-specific ablation of von Hippel-Lindau protein (VHL(fl/fl)) in mice. (ox.ac.uk)
  • This type of injury impairs mitochondrial function and leads to cell death, which impairs cardiac function and negatively affects patient outcome [1]. (oroboros.at)
  • HIF-1 reduces ischaemia-reperfusion injury in the heart by targeting the mitochondrial permeability transition pore. (ox.ac.uk)
  • Mechanistically this is accompanied by preservation of myocardial PPARα activity in AGS, which is significantly downregulated in the rat, and a metabolic phenotype consistent with the development of mitochondrial substrate flux "bottlenecks" in rats (myocardial accumulation of acylcarnitines and ceramides, organic acid profiles consistent with compromised citric acid cycle flux) compared to AGS. (duke.edu)
  • Cardiac cells that survive this first wave of injuries will often have their mitochondrial functions compromised, and this can lead to further dysfunction and even cellular death. (prohealth.com)
  • The authors carried out tests on an animal model to investigate the individual and combined effects of melatonin and NMN on myocardial function, mitochondrial activity, and oxidative stress status following ischemia/reperfusion injury in aged rat hearts. (prohealth.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)
  • AIMS: Hypoxia-inducible factor-1 (HIF-1) has been reported to promote tolerance against acute myocardial ischaemia-reperfusion injury (IRI). (ox.ac.uk)
  • The downstream regulator of PI3K/Akt is hypoxia-inducible factor-1α (HIF-1α) which is a master regulator of gene expression in hypoxia, and it has the ability to influence cellular adaptive responses to hypoxia or ischemia. (springeropen.com)
  • Heusch G: Molecular basis of cardioprotection: Signal transduction in ischemic pre-, post-, and remote conditioning. (spandidos-publications.com)
  • The molecular events by which this precisely controlled increased reliance on myocardial FA utilization is cardioprotective in hibernators while it adversely impacts post-I/R cardiac efficiency and function in non-hibernators represent a significant knowledge gap. (duke.edu)
  • Here we investigated the molecular signals of the ischemia non-affected remote lateral and posterior regions and present gene expression profiles of the entire left ventricle by using our novel and straightforward method of 2D and 3D image reconstruction. (oncotarget.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)
  • 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)
  • Pretreating the rats with simvastatin 18 hour prior to the induction of ischemiareperfusion has been shown to reduce cardiac dysfunction and improve coronary flow [ 7 ]. (ac.ir)
  • In heart transplantation, donor hearts inevitably suffer from ischemia/reperfusion (I/R) injury, which leads to primary graft dysfunction and affects patients' survival rate. (researchsquare.com)
  • Finding all 3 entities in the same patient with chronic myocardial dysfunction is not uncommon (see the image above). (medscape.com)
  • These results showed that DOEO had significant myocardial cell protection, with IC 50 values ranging from 17.64 to 24.78 μg/mL in vitro . (wjtcm.net)
  • MATERIALS AND METHODS: Establish an in vitro radiation injury model by irradiating GC-2spd cells with 60Co γ-rays (4 Gy or 8 Gy). (bvsalud.org)
  • Bone marrow mesenchymal stem cells (BMSCs) have been reported to attenuate myocardial I/R injury via their paracrine effects, which can be enhanced by hypoxic preconditioning. (researchsquare.com)
  • In today's paper, first author Dr Valiente-Alandi, corresponding author Dr Blaxall from University of Cincinnati College of Medicine and Heart Institute, and their colleagues hypothesized that interfering with fibronectin polymerization, or its genetic ablation and fibroblasts, would attenuate myocardial fibrosis and improve cardiac function following ischemia reperfusion injury. (libsyn.com)
  • 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)
  • Endothelial injury can trigger activation of the complement system, promoting inflammation and the development of endothelial injury syndromes, ultimately leading to organ damage and failure. (biomedcentral.com)
  • The concomitant presence of myocardial necrosis with myocardial ischemia, stunning, or hibernation may complicate appraisal of left ventricular (LV) function and patient management. (medscape.com)
  • Several imaging modalities have been proposed for accurate assessment of myocardial necrosis, viability, stunning, and hibernation, with mixed results. (medscape.com)
  • 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)
  • Protection of the heart against injury from acute ischemia remains challenging for emergency physicians and cardiologists because there are no therapies proven to directly protect the heart against the deleterious effects of ischemia in humans. (mcw.edu)
  • 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)
  • Overall, the study showed that DOEO displayed myocardial protection by upregulating the NF-E2-related nuclear factor- antioxidant response element (Nrf2-ARE) and caspase pathways. (wjtcm.net)
  • Abouzaki NA, Christopher S, Trankle C, Van Tassell BW, Carbone S, Mauro AG, Buckley L, Toldo S and Abbate A: Inhibiting the inflammatory injury after myocardial ischemia reperfusion with plasma-derived Alpha-1 Antitrypsin: A post hoc analysis of the VCU-α1RT study. (spandidos-publications.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)
  • Using a clinically relevant model of surgical deep hypothermic circulatory arrest (DHCA) combined with targeted metabolomic and proteomic profiling, we are investigating how changes in hibernation-specific myocardial expression/activity of PPARα nuclear receptor and downstream target genes (FGF21) following cardiac surgery can provide cardioprotection by increasing myocardial fatty acid oxidation and inhibiting NF-κB regulated pro-inflammatory responses. (duke.edu)
  • When blood flow is re-established (reperfusion), a series of inflammatory responses take place because of the damage sustained by the tissues affected by the previous lack of blood. (prohealth.com)
  • Endothelial injury triggers activation of the complement system-significantly through the lectin pathway-via altered cell-surface patterns on injured endothelial cells, initiating an inflammatory response [ 7 ]. (biomedcentral.com)
  • The cardioprotective effects of DOEO were examined by histopathological observation, myocardial enzyme detection, peroxidation, anti-oxidant level detection, and related protein expression. (wjtcm.net)
  • Research done in animals shows that treatment with NAD+ precursors like NMN have cardioprotective effects against ischemia/reperfusion injury (4). (prohealth.com)
  • Numerous apoptotic cardiomyocytes were found in ischemic fields in ischemia-reperfusion groups and werent observed in the sham-operated group. (ac.ir)
  • The initial ischemia in AMI causes biochemical and metabolic alterations in cardiomyocytes. (springeropen.com)
  • The lack of effective treatments to reduce the consequences of myocardial ischemia-reperfusion injury and the increased reliance on percutaneous and surgical treatments for coronary and valvular disease or end-stage heart failure make it critically important to identify new targets and strategies for cardioprotection. (duke.edu)
  • This study aimed to determine the potential myocardial protective effect and possible mechanism of action of D. odorifera essential oil (DOEO). (wjtcm.net)
  • BACKGROUND: Dexmedetomidine (DEX), a specific α2-adrenergic receptor agonist, is protective against myocardial ischemia/reperfusion injury (MIRI). (bvsalud.org)
  • Inhibiting fibronectin matrix deposition by pUR4 treatment or by deleting fibronectin gene expression in cardiac fibroblasts confirmed cardioprotection against ischemia reperfusion-induced injury by attenuating at first left ventricular remodeling and cardiac fibrosis, thus preserving cardiac function. (libsyn.com)
  • However, there yet remain unknown aspects of MIRI and cardioprotection, and in Figure 1 , we present a briefly summarized conceptual diagram of the pathophysiology of MIRI involving the parts mentioned above. (hindawi.com)
  • 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)
  • siRNA knockdown of PKN1 in NRVM significantly decreased cell survival and increased cell injury by sI/R which was reversed by WT- or KD-PKN1 expression. (figshare.com)
  • Moreover, it was observed that, PGRN protects the heart against ischemia-reperfusion injury. (biomedcentral.com)
  • We have previously shown that intralipid (lipid emulsion) protects the heart against ischemia/reperfusion injury and bupivacaine-induced cardiotoxicity. (asahq.org)
  • Most myocardial infarctions, commonly known as heart attacks, happen in people once they get older, and aging makes it more difficult to recover from this type of injury. (prohealth.com)
  • Fibronectin polymerization is necessary for collagen matrix deposition and is a key contributor to increased abundance of cardiac myofibroblast following cardiac injury. (libsyn.com)
  • Hibernators such as arctic ground squirrels (AGS) depress their metabolic, heart, and respiratory rates as well as their core body temperature to enter a state called torpor during which they exhibit remarkable resistance to myocardial I/R injury and ventricular dysrhythmias normally associated with hypothermia. (duke.edu)
  • Interestingly, this winter cardioprotective phenotype is associated not only with suppression of metabolic demand, but also with a fuel shift from myocardial carbohydrate to fatty acid (FA) metabolism. (duke.edu)
  • While the heart is capable of utilizing a variety of available substrates to generate adenosine triphosphate, this metabolic flexibility is compromised under circumstances in which the heart is stressed, particularly by myocardial ischemia. (biomedcentral.com)
  • Insulin, glucose and potassium (GIK) are touted as useful metabolic adjuvant, associated with improvement of cardiac function in acute myocardial function, but the general acceptance of this therapeutic approach is limited by requirements for concomitant infusion of glucose and concerns regarding hypoglycemia. (biomedcentral.com)
  • We have reported that retrograde application of embryonic endothelial progenitor cells (eEPCs) provides rapid paracrine protection against ischemia-reperfusion injury. (elsevierpure.com)
  • The Institute has made extraordinary contributions in many fields, particularly myocardial ischemia/reperfusion injury, cardioprotection, environmental cardiology, diabetes, heart failure, stem cells, and regenerative cardiology and performed the first study of cardiac stem cells in humans. (uoflhealth.org)
  • Reperfusion injury increases the damage done after events such as heart attacks. (prohealth.com)
  • We show in exercised mice that the expression of CITED4, a transcriptional co-regulator necessary for cardioprotection, is regionally heterogenous in the heart with preferential significant increases in the lateral wall compared with sedentary mice. (researchgate.net)
  • Ischaemia-reperfusion (I/R) injury is the most important and common cause of myocardial damage and subsequent heart failure worldwide ( 1 , 2 ). (spandidos-publications.com)
  • Systolic wall thickening after coronary artery occlusion and subsequent reperfusion in normal and ischemic zones. (medscape.com)
  • Furthermore, the hibernator cardioprotective phenotype is also associated with reduced myocardial NF-κB activity, reduced expression of downstream cytokines and neutrophil extravasation following cardiac surgery. (duke.edu)
  • We feel that developing strategies to help 'switch' myocardial metabolism to resemble that naturally occurring in mammalian hibernators represents a transformative approach that could ultimately have an important positive impact in patients undergoing cardiac surgery and transplantation, as well as in victims of cardiac arrest, stroke, trauma and hypothermia, in addition to fundamentally advancing the field of nuclear receptor biology and myocardial substrate metabolism under extremes of physiology. (duke.edu)
  • Background-Prolonged myocardial ischemia results in cardiomyocyte loss despite successful revascularization. (elsevierpure.com)
  • Recovery of myocardial contractile function after spontaneous restoration of flow may be protracted similarly after angioplasty or revascularization surgery. (medscape.com)
  • Multitarget Strategies to Reduce Myocardial Ischemia/Reperfusion Injury: JACC Review Topic of the Week. (nih.gov)
  • However, clinical and preclinical results using various cardioprotective strategies to attenuate reperfusion injury have generally not been applicable for every day clinical practice. (eurekaselect.com)
  • Here we discuss evidence for the role of lectin pathway activation in endothelial injury-associated complications of HSCT and how targeting complement activity may provide therapeutic benefit for patients with HSCT-TMA. (biomedcentral.com)
  • Regional myocardial function and electrophysiological alteration after coronary artery occlusion. (medscape.com)
  • We have previously shown that distal anterior wall ischemia/reperfusion induces gene expression changes in the proximal anterior myocardial area, involving genes responsible for cardiac remodeling. (oncotarget.com)
  • 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)