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Myocardial Reperfusion InjuryReperfusion InjuryMyocardial IschemiaIschemic Preconditioning, MyocardialMyocardiumMyocardial ReperfusionIschemic PostconditioningCardiotonic AgentsIschemiaMyocardial InfarctionMyocytes, CardiacReperfusionRats, Sprague-DawleyDisease Models, AnimalBrain IschemiaPeroxidaseL-Lactate DehydrogenaseCreatine KinaseApoptosisHeartIschemic PreconditioningRats, WistarMice, Inbred C57BLReceptor, Adenosine A3Ventricular Function, LeftHeart Function TestsMitochondria, HeartMice, KnockoutTime FactorsOxidative StressHemodynamicsMyocardial ContractionNitric OxideSignal TransductionWarm IschemiaProto-Oncogene Proteins c-aktNitric Oxide Synthase Type IICoronary CirculationProtective AgentsNitric Oxide Synthase Type IIICold IschemiaMalondialdehydeNecrosisReactive Oxygen SpeciesAntioxidantsNeutrophilsDogsKidneyPerfusionPeroxynitrous AcidNeutrophil InfiltrationRabbitsCytoprotectionCaspase 3Random AllocationLiverCoronary VesselsNeuroprotective AgentsCyclic S-OxidesKATP ChannelsAcute Kidney InjuryIn Situ Nick-End LabelingConstrictionBlotting, WesternSwineEnzyme InhibitorsInfarction, Middle Cerebral ArterySuperoxide DismutaseWounds and InjuriesTroponin IAspartate AminotransferasesSpinal Cord IschemiaOrgan PreservationModels, AnimalIschemic Attack, TransientArrhythmias, CardiacAlanine TransaminaseTumor Necrosis Factor-alphaOrgan Preservation SolutionsHeme Oxygenase-1Heart RateCells, CulturedBlood PressureMyocardial StunningTioproninHeart VentriclesElectrocardiographyCoronary DiseaseHydroxy AcidsDecanoic AcidsRats, Inbred LewFree Radical ScavengersSuperoxidesMicrocirculationDose-Response Relationship, DrugAdenosineMice, TransgenicEndothelium, VascularCardioplegic SolutionsLiver Diseases
InhibitionIschemicCardiacMyocardiumProtectsRatsAcute myocardialMiceCoronary diseaseDysfunctionSignalling pathwayInfarction sizeMitophagyNrf2CardiomyocytesVitroHypoxiaInflammationCardioprotectionApoptosisAttenuatesCardioprotective EffectsDiabeticMTORC1IntracellularVentricularResponsesGlucose oxidationEnzymesPathwaysKinaseProtective effectTumorSignificantlyNLRP3ArrhythmiasHepaticImpairmentImportantlyCellularContributesModelComplementSubstrateHeartProteinMechanismsProteinsProtectionClinical
Inhibition5
  • 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)
  • Inhibition of Caspase-1 Activation in Endothelial Cells Improves Angiogenesis: A NOVEL THERAPEUTIC POTENTIAL FOR ISCHEMIA. (immunochemistry.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)
  • 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)
Ischemic8
  • AMPK has emerged as a pertinent stress-activated kinase that has been shown to have cardioprotective capabilities against myocardial ischemic injury. (nih.gov)
  • To determine whether ischemic AMPK activation-modulated by the Sesn2-AMPK complex in the heart-is impaired in aging that sensitizes the heart to ischemic insults, young C57BL/6 mice (age 3-4 mo), middle-aged mice (age 10-12 mo), and aged mice (age 24-26 mo) were subjected to left anterior descending coronary artery occlusion for in vivo regional ischemia. (nih.gov)
  • Furthermore, Sesn2-knockout hearts demonstrate a cardiac phenotype and response to ischemic stress that is similar to wild-type aged hearts ( i.e., impaired ischemic AMPK activation and higher sensitivity to ischemia- and reperfusion- induced injury). (nih.gov)
  • therefore, Sesn2 is a scaffold protein that mediates AMPK activation in the ischemic myocardium via an interaction with AMPK upstream LKB1. (nih.gov)
  • D. odorifera may be a potential candidate drug for treating myocardial ischemic injury. (wjtcm.net)
  • The re-establishing of blood flow to an ischemic zone is called reperfusion [ 1 ]. (biomedcentral.com)
  • Because of the increased ability of the immature myocardium to rely on anaerobic glycolysis, it can withstand ischemic injury better than adult myocardium can. (medscape.com)
  • The ischemic injury underlying these illnesses is complex, involving intricate interplays among many biological functions including energy metabolism, vascular regulation, hemodynamics, oxidative stress, inflammation, platelet activation, and tissue repair that take place in a context- and time-dependent manner. (cdc.gov)
Cardiac12
  • Cardiac Toll-like receptors and inflammasome complexes may be key inducers for inflammation probably through NF- B activation and ROS overproduction. (hindawi.com)
  • Activation of Toll-like receptors (TLRs) and the inflammasome complex has recently been proposed to be central in cardiac inflammation and likely in the pathogenesis of DCM. (hindawi.com)
  • GRh2 reduced the area of myocardial infarction and the histological changes in the myocardium and improved cardiac functions. (spandidos-publications.com)
  • Immunoprecipitation with Sesn2 Ab revealed that cardiac Sesn2 forms a complex with AMPK and upstream liver kinase B1 (LKB1) during ischemia. (nih.gov)
  • Rapid recovery of the blocked coronary flow represents the most effective strategy to reduce the size of myocardial infarction and improve the cardiac function. (edu.iq)
  • Wild‐type C57BL/6J mice (male, 8-10 weeks old) were used and murine myocardial ischemia and reperfusion injury (IRI) model was conducted, cardiac function was evaluated by echocardiography. (edu.iq)
  • DEX preconditioning significantly improved cardiac dysfunction reduced myocardial infarction size, maintained mitochondrial structural integrity, increased mitochondrial membrane potential, inhibited autophagosomes formation, and decreased ROS production and Beclin1, LC3II/I ratio, PINK1, Parkin, and p62 expression(p (bvsalud.org)
  • The accumulation of cardiac lactate was attenuated by PLCA during myocardial I/R, and infarct size was smaller in rats treated with PLCA (1 mg/kg) than in those treated with caffeic acid (1 mg/kg). (biomedcentral.com)
  • 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)
  • This change has been linked to activation of energy-consuming processes, which leads to decreased levels of adenosine triphosphatase (ATP) and a subsequent lack of energy sources for healthy cardiac function. (medscape.com)
  • Consequences depend on degree and location of obstruction and range from unstable angina to non-ST-segment elevation myocardial infarction (NSTEMI), ST-segment elevation myocardial infarction (STEMI), and sudden cardiac death. (msdmanuals.com)
  • These syndromes all involve acute coronary ischemia and are distinguished based on symptoms, ECG findings, and cardiac marker levels. (msdmanuals.com)
Myocardium3
Protects1
  • Moreover, it was observed that, PGRN protects the heart against ischemia-reperfusion injury. (biomedcentral.com)
Rats3
  • 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)
  • CONCLUSION: Therefore, DEX preconditioning was cardioprotective against MIRI in rats by suppressing mitophagy via α2-adrenergic receptor activation. (bvsalud.org)
  • We aimed to investigate the effect of PLCA on hypoxia/reoxygenation (H/R) in neonatal rat ventricular myocytes (NRVM) and on myocardial I/R in rats. (biomedcentral.com)
Acute myocardial4
Mice3
  • Beneficial effects of IL-37 after spinal cord injury in mice. (nature.com)
  • 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)
Coronary disease1
Dysfunction2
  • There is evidence that chronic progression of hypertrophy, fibrosis, and ventricular dysfunction is correlated with a local increase in cytokines [ 16 ] and activation of NF- B [ 17 , 18 ]. (hindawi.com)
  • These factors affect the way in which the immature heart handles calcium, which, in turn, contributes to the myocardial dysfunction observed after CPB. (medscape.com)
Signalling pathway1
Infarction size1
Mitophagy1
  • OBJECTIVE: Hence, we aimed to investigate whether DEX preconditioning alleviates MIRI by suppressing mitophagy via α2-adrenergic receptor activation. (bvsalud.org)
Nrf23
  • 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)
  • 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)
  • 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)
Cardiomyocytes5
  • Inflammatory signaling in cardiomyocytes usually occurs as an early response to myocardial injury and entails cytosolic and mainly mitochondrial reactive oxygen species (ROS) overproduction [ 10 , 11 ]. (hindawi.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)
  • Vascular endothelial cell (EC)-derived factors play an important role in endothelial-cardiomyocyte crosstalk and could save cardiomyocytes (CMs) from injury. (mdpi.com)
  • Cardiomyocytes were isolated and subjected to 6 h hypoxia followed by 18 h reperfusion. (biomedcentral.com)
  • The initial ischemia in AMI causes biochemical and metabolic alterations in cardiomyocytes. (springeropen.com)
Vitro2
  • 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)
  • 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)
Hypoxia3
  • Recent evidence obtained in mouse models shows its essential role regulating blood cell function through various mechanisms that include pseudohypoxia responses by hypoxia-inducible factor-1α activation, post-translational modifications like succinylation, and communication mediated by succinate receptor 1. (haematologica.org)
  • 6 3 In fact, one of the first pieces of evidence for a role of succinate in cancer development was provided by the discovery of pseudohypoxia, which refers to activation of hypoxia signaling pathways under normal oxygen levels. (haematologica.org)
  • 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)
Inflammation3
  • We and others have reported that myocardial inflammation develops in human patients and experimental models of type 1 (T1DM) and type 2 (T2DM) diabetes mellitus [ 8 , 14 , 15 ]. (hindawi.com)
  • Myocardial protection was associated with reduced markers of systemic and local inflammation, including cytokine contents (interleukin-1 and KC) and myeloperoxidase activity. (ox.ac.uk)
  • 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)
Cardioprotection2
  • Heusch G: Myocardial ischaemia-reperfusion injury and cardioprotection in perspective. (spandidos-publications.com)
  • Here, we show that in a mouse model of chronic neuropathic pain, ischemia-reperfusion injury following myocardial infarction is reduced, and this cardioprotection is induced via an anterior nucleus of paraventricular thalamus (PVA)-dependent parasympathetic pathway. (sinica.edu.tw)
Apoptosis3
Attenuates2
  • The aim of the study is to investigate the effects of curcumin in attenuates myocardial ischemia and reperfusion-induced proinflammatory response through activation of the Nrf-2/HO-1 signaling pathway. (edu.iq)
  • Inconclusion, this study demonstrates that curcumin attenuates myocardial IRI by inhibiting proinflammatory cytokines through a mechanism that may be related to activation of the Nrf-2/HO-1 signaling pathway. (edu.iq)
Cardioprotective Effects1
  • The cardioprotective effects of DOEO were examined by histopathological observation, myocardial enzyme detection, peroxidation, anti-oxidant level detection, and related protein expression. (wjtcm.net)
Diabetic1
  • Here we review the current literature on scutellarin to provide a comprehensive understanding of the pharmacological activity, mechanism of action, toxicity, and therapeutic potential of scutellarin for the treatment of ischemia, diabetic complications, and other chronic diseases. (cdc.gov)
MTORC11
  • Downregulation of LAPTM4B Contributes to the Impairment of the Autophagic Flux via Unopposed Activation of mTORC1 Signaling During Myocardial Ischemia/Reperfusion Injury. (nih.gov)
Intracellular1
  • Intracellular mature form of IL-37, but not its extracellular form, markedly inhibited migration of multiple kinds of tumor cells through inhibiting Rac1 activation. (nature.com)
Ventricular1
  • Subsequent disruption of calcium homeostasis and myocardial remodeling leads to a progressive impairment of ventricular myocyte contractility that may result in heart failure [ 6 - 8 ]. (hindawi.com)
Responses1
  • The resulted data showed that curcumin alleviates myocardial inflammatory responses and oxidative stress during myocardial IRI. (edu.iq)
Glucose oxidation1
  • The uncoupling of glycolysis and glucose oxidation induces lactate accumulation during myocardial ischemia/reperfusion (I/R) injury. (biomedcentral.com)
Enzymes4
  • 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)
  • 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)
  • Abnormal and uncontrolled activation of these enzymes lead to cellular damage after CPB. (medscape.com)
Pathways1
  • Nonetheless, when cells rely on anaerobic glycolysis, like cancer cells and certain innate immune cells upon activation, other metabolic pathways sustain succinate levels, including glutamine-dependent anerplerosis to α-ketoglutarate, and eventually citrate by reductive carboxylation. (haematologica.org)
Kinase1
Protective effect2
  • This study aimed to determine the potential myocardial protective effect and possible mechanism of action of D. odorifera essential oil (DOEO). (wjtcm.net)
  • Facilitation of glucose utilization contributes to the protective effect of AKT signaling to reduce infarct size and improve myocardial function in a heart subjected to I/R [ 15 ]. (biomedcentral.com)
Tumor1
  • The initiation and development of tumor cell is accompanied by elevated stresses, such as oncogene activation, DNA damage, genome instability, and reprogrammed tumor metabolism. (nature.com)
Significantly3
  • miR‑132 was significantly upregulated and SIRT1 was markedly downregulated in I/R myocardial tissues. (spandidos-publications.com)
  • 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)
  • 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)
NLRP31
  • Ginsenoside Rg3 Ameliorates DSS-Induced Colitis by Inhibiting NLRP3 Inflammasome Activation and Regulating Microbial Homeostasis. (immunochemistry.com)
Arrhythmias1
Hepatic1
  • Hematopoietic stem cell transplantation and associated risk factors precipitate endothelial injury, leading to HSCT-TMA and other endothelial injury syndromes such as hepatic veno-occlusive disease/sinusoidal obstruction syndrome, idiopathic pneumonia syndrome, diffuse alveolar hemorrhage, capillary leak syndrome, and graft-versus-host disease. (biomedcentral.com)
Impairment1
Importantly2
  • In this sense, it has been shown that TLR2 participated importantly in the mechanism of ROS-induced activation of NF- B and AP-1 [ 24 ]. (hindawi.com)
  • Importantly, delayed myocardial damage as measured 24 h post-reperfusion was equally protected by administration of 10 microg MTII. (ox.ac.uk)
Cellular1
  • Platelets migrate to the area of injury, where they secrete several cellular factors and mediators. (medscape.com)
Contributes1
  • Neutrophil infiltration and activation contributes to tissue damage, via the release of myeloperoxidase (MPO) and formation of the damaging oxidant hypochlorous acid. (ku.dk)
Model4
  • A rat model of myocardial I/R injury was constructed by ligating the left anterior descending coronary artery, which was subsequently treated with GRh2. (spandidos-publications.com)
  • Caspase-1 Activation Is Related With HIV-Associated Atherosclerosis in an HIV Transgenic Mouse Model and HIV Patient Cohort. (immunochemistry.com)
  • Here we exploited the potential protective role that melanocortin receptor type 3 (MC3-R) activation might play in a myocardial ischemia-reperfusion injury model. (ox.ac.uk)
  • Objectives: We sought to determine proteasome adequacy in I/R hearts, create a mouse model of cardiomyocyte-restricted PSMI (CR-PSMI), and test CR-PSMI impact on I/R injury. (elsevierpure.com)
Complement3
  • Together, activation of complement and the coagulation cascade lead to a procoagulant state that may result in development of HSCT-TMA. (biomedcentral.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)
  • As such, new drugs that would complement reperfusion by providing neural and cardiovascular protection and by targeting multiple abnormalities in ischemia are receiving increased attention. (cdc.gov)
Substrate1
  • These data indicate that elevated levels of the MPO substrate SCN-, which can be readily modulated by dietary means, can protect against acute ischemia-reperfusion injury. (ku.dk)
Heart6
  • 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)
  • Coronary heart disease is a leading cause of death in the world and therapy to reduce injury is still needed. (biomedcentral.com)
  • In resting conditions, mouse and rat heart extracts expressed MC3-R mRNA and protein, without changes following ischemia-reperfusion. (ox.ac.uk)
  • In vivo, administration of the melanocortin agonist MTII (10 microg per mouse equivalent to 9.3 nmol) 30 min prior to ischemia (25 min) attenuated mouse heart 2 h reperfusion injury by approximately 40%, an effect prevented by the mixed MC3/4-R antagonist SHU9119 but not by the selective MC4-R antagonist HS204. (ox.ac.uk)
  • In conclusion, this study has highlighted a previously unrecognized protective role for MC3-R activation on acute and delayed heart reperfusion injury. (ox.ac.uk)
  • These data may open new avenues for therapeutic intervention against heart and possibly other organ ischemia-reperfusion injury. (ox.ac.uk)
Protein1
  • When β3-AR are coupled with Gi protein they can act as a brake on β1- and β2 adrenergic receptors to prevent over-activation by opposing the classical inotropic effect of β1 and β2 adrenergic receptors. (wikipedia.org)
Mechanisms4
  • 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)
  • MC-3 receptor and the inflammatory mechanisms activated in acute myocardial infarct. (ox.ac.uk)
Proteins1
  • Supplementation also decreased antibody recognition of HOCl-damaged myocardial proteins. (ku.dk)
Protection2
  • Above all, PGRN also provides protection in the initial phase following myocardial ischemia-reperfusion injury. (biomedcentral.com)
  • [ 3 , 4 ] Further refinements in CPB hardware and techniques, perfusion methods, myocardial and brain protection over the past seven decades contributed to improved outcomes of surgical treatment of CHD. (medscape.com)
Clinical2