AnatomyOrganismsDiseasesChemicals and DrugsAnalytical, Diagnostic and Therapeutic Techniques and EquipmentPhenomena and ProcessesDisciplines and OccupationsInformation ScienceHealth Care
Myocardial Reperfusion InjuryReperfusion InjuryMyocardial IschemiaMyocardial ReperfusionIschemic PostconditioningMyocardiumMyocardial InfarctionCardiotonic AgentsIschemic Preconditioning, MyocardialMyocytes, CardiacCreatine KinaseRats, Sprague-DawleyHeartDisease Models, AnimalPeroxidaseReperfusionIschemiaCoronary CirculationHemodynamicsVentricular Function, LeftRats, WistarMyocardial ContractionCardioplegic SolutionsHeart Function TestsL-Lactate DehydrogenaseApoptosisMice, Inbred C57BLMitochondria, HeartTime FactorsReceptor, Adenosine A3Ischemic PreconditioningMice, KnockoutDogsOxidative StressBrain IschemiaRandom AllocationNeutrophilsWounds and InjuriesP-SelectinSignal TransductionNitric OxideProto-Oncogene Proteins c-aktNitric Oxide Synthase Type IINitric Oxide Synthase Type IIICoronary VesselsElectrocardiographyWarm IschemiaProtective AgentsNecrosisPerfusionMalondialdehydeRabbitsBrain InjuriesCold IschemiaArrhythmias, CardiacSwineHeart Arrest, InducedAntioxidantsPeroxynitrous AcidNeutrophil InfiltrationKidneyTroponin IReactive Oxygen SpeciesAcute Kidney InjuryHeart VentriclesHeart RateCytoprotectionLiverCaspase 3ThrombectomyBlood PressureModels, AnimalBlotting, WesternKATP ChannelsAngioplasty, Balloon, CoronaryEnzyme InhibitorsMicrocirculationIn Situ Nick-End LabelingCells, CulturedCoronary AngiographyOrgan PreservationSuperoxide DismutaseVentricular PressureCyclic S-OxidesEchocardiographyConstrictionSuctionCoronary DiseaseTumor Necrosis Factor-alphaOrgan Preservation SolutionsAspartate AminotransferasesMitochondrial Membrane Transport ProteinsAthletic InjuriesAlanine TransaminaseCreatine Kinase, MB FormEndothelium, VascularTreatment OutcomeSpinal Cord InjuriesMice, TransgenicRats, Inbred Lew
InfarctionOxidative stressApoptosisMyocardiumDysfunctionInhibitionTherapeuticCardioprotectionInfarctTroponinMyocytesCardioprotective effectsRelease of myocardialMorbidity and mortaRatsSignificantlyHypoxiaCardiomyocytesProtectiveContributesVitroPathologicalIsoproterenolMesenchymal stemFibrosisIntracellular calciumCytokinesMechanismsMurineFibroblastsLactate dehydrogenaseVivoBiomarkersVentricularProtectsPathophysiologyOxidationHeartDiabeticEndogenousAnti-inflammatory effectsNrf2DiastolicCardiovascular diseasesPatientsEndothelialCoronary arteryProinflammatoryBone marrow-derivedClinicalArrestInflammatory responsePathwaysMitochondrial functionMethodsHydrogen
Infarction29
Oxidative stress14
  • 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)
  • 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 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)
  • Cardiac oxidative stress and local inflammation were measured by detecting the levels of malondialdehyde, enzymatic antioxidant status and proinflammatory cytokines. (kjpp.net)
  • It was observed that mangiferin ameliorated D-galactose-induced cardiac aging, attenuated cardiac oxidative stress, inflammation and fibrosis, as well as inhibited the activation of TGF-β1/p38/MK2 signaling pathway. (kjpp.net)
  • Infarct size measurement, cardiac troponin-I assays, oxidative stress analysis and histopathological analyzed. (edu.iq)
  • The resulted data showed that curcumin alleviates myocardial inflammatory responses and oxidative stress during myocardial IRI. (edu.iq)
  • These signaling pathways regulate a variety of physiological and molecular processes throughout the body 10 -processes that have an impact on key biomarkers of aging , such as mitochondrial function 11-16 and cellular defense against oxidative stress. (lifeextension.com)
  • In parallel, antioxidant activity and sequestration of oxidized molecules provided by HDL can attenuate the oxidative stress that triggers ischemia/reperfusion. (unipr.it)
  • Post-resuscitation myocardial injury is evidently due to oxidative stress, calcium overload, neutrophil accumulation, microvascular damage, and abnormal energy metabolism, among other causes. (dirjournal.org)
  • 1,2,3 As one of the most common pathological mechanisms after the ROSC, energy metabolism disorder in the myocardium leads to a series of detrimental changes in the energy supply and substrate metabolism related to the regulation of mitochondrial function, oxidative stress, and inflammation. (dirjournal.org)
  • To provide in vivo evidence that DJ‑1 is involved in the delayed cardioprotection induced by ischemic preconditioning (IPC) against oxidative stress caused by ischemia/reperfusion (I/R), the present study subjected male Sprague‑Dawley rats to IPC (3 cycles of 5‑min coronary occlusion/5‑min reperfusion) 24 h prior to I/R (30‑min coronary occlusion/120‑min reperfusion). (spandidos-publications.com)
  • However, in situ knockdown of DJ‑1 attenuated the IPC‑induced delayed cardioprotection, and reversed the inhibitory effect of IPC on I/R‑induced oxidative stress. (spandidos-publications.com)
  • Subsequent research suggested that DJ-1 has various potential functions, including transcriptional regulation, oxidative stress inhibition, acting as a chaperone or protease and mitochondrial regulation ( 12 ). (spandidos-publications.com)
Apoptosis11
  • 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)
  • Reports showed that mangiferin administration ameliorated isoproterenol-induced apoptosis [ 12 ] and hydrogen peroxide-induced cell injury [ 10 ] in cardiomyocytes. (kjpp.net)
  • These protective effects may be associated with the inhibition of apoptosis and inflammation, as reflected by less TUNEL-positive cells and lower levels of serum proinflammatory cytokines (Interleukin-1β, Interleukin-6, tumor necrosis factor-α) and cardiac troponin I in the N-CM group compared with the vehicle group. (researchsquare.com)
  • All of these factors are known to result in myocardial apoptosis(5) and the acceleration of allograft rejection or chronic allograft dysfunction. (researchsquare.com)
  • Also, curcumin reduces cell apoptosis induced by myocardial IRI, curcumin reduces cell apoptosis induced by myocardial IRI and activates the Nrf-2/HO-1 signaling pathway during myocardial. (edu.iq)
  • Our study provides a new method to tackling apoptosis related cardiac diseases. (molcells.org)
  • Furthermore, ADSCs secrete a series of paracrine factors to promote neovascularization, reduce apoptosis, and inhibit fibrosis, which contributes to cardiac regeneration. (biomedcentral.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)
  • 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)
  • In addition, PEMF treatment also reduced the apoptosis of myocardial cells by up-regulating the expression of anti-apoptosis protein B-cell lymphoma 2 (Bcl-2) and down-regulating the expression of pro-apoptosis protein (Bax). (pemfglobal.com)
Myocardium13
  • However, whether GRh2 has a protective effect on ischaemia/reperfusion (I/R) in the myocardium has yet to be elucidated. (spandidos-publications.com)
  • 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)
  • 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)
  • BACKGROUND: Coagulation disorders and reperfusion of ischemic myocardium are major causes of morbidity and mortality. (regionh.dk)
  • 7 The metabolism of fatty acids and glucose undergoes adaptive changes in the myocardium due to ischemia-reperfusion injury after cardiopulmonary resuscitation (CPR). (dirjournal.org)
  • These pleiotropic effects thus have a major role in protecting the myocardium against ischemic injury. (ac.ir)
  • In addition treatment with T. terrestris decreased the leakage of CK-MB and LDH enzymes from myocardium, there was a significant improvement in cardiac function as evidenced by correction of MAP, HR, LVEDP and contractility and relaxation. (scialert.net)
  • 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)
  • Immature calcium handling in immature myocardium raises intracellular calcium concentrations after ischemia and reperfusion. (medscape.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)
Dysfunction16
  • 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 role of cardiac proteasome dysfunction during I/R and the perspective to diminish I/R injury by manipulating proteasome function remain unclear. (elsevierpure.com)
  • Euthyroid sick syndrome (also known as nonthyroidal illness syndrome) can be described as abnormal findings on thyroid function tests that occur in the setting of a nonthyroidal illness (NTI), without preexisting hypothalamic-pituitary and thyroid gland dysfunction. (medscape.com)
  • Lipoic acid increases the abundance of other protective antioxidants while improving mitochondrial function and preventing glycation-induced damage in the kidney and blood vessels of those with diabetes-thus defending against diabetic kidney disease, vision loss, and vascular dysfunction. (lifeextension.com)
  • 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)
  • A wealth of studies now confirm that PQQ's cell-signaling activity translates into substantial protection against degenerative and age-related conditions, such as mitochondrial dysfunction, 1 heart degeneration, 18-20 brain injury, and cognitive decline. (lifeextension.com)
  • To investigate the feasibility and usefulness of 2-deoxy-2-( 18 F)-fluoro-D-glucose positron emission tomography/computed tomography [( 18 F)-FDG PET/CT] as a novel examination in the surveillance of abnormal myocardial energy metabolism and cardiac dysfunction after cardiopulmonary resuscitation (CPR). (dirjournal.org)
  • Myocardial dysfunction remains a leading problem in the early period following the return of spontaneous circulation (ROSC) after cardiac arrest. (dirjournal.org)
  • Some in vitro experiments demonstrated that early intervention in cardiac metabolism disorder attenuated myocardial damage and dysfunction. (dirjournal.org)
  • 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)
  • Cardiac dysfunction was observed as a decrease in mean arterial pressure (MAP), heart rate (HR), left ventricular rate of peak positive and negative pressure change {(+) and (-) LV dP/dt} and elevated left ventricular end diastolic pressure (LVEDP) following ISP administration. (scialert.net)
  • Dynamin-related protein 1 (Drp1)-mediated diastolic dysfunction in myocardial ischemia-reperfusion injury: therapeutic benefits of Drp1 inhibition to reduce mitochondrial fission. (uchicago.edu)
  • Ischemia-induced Drp1 and Fis1-mediated mitochondrial fission and right ventricular dysfunction in pulmonary hypertension. (uchicago.edu)
  • ROS promote epigenetic remodeling and cardiac dysfunction in offspring following maternal engineered nanomaterial (ENM) exposure. (wvu.edu)
  • Reactive oxygen species damage drives cardiac and mitochondrial dysfunction following acute nano-titanium dioxide inhalation exposure. (wvu.edu)
  • All of 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)
Inhibition5
  • Rationale: Both cardiomyocyte-restricted proteasome functional enhancement and pharmacological proteasome inhibition (PSMI) were shown to attenuate myocardial ischemia/reperfusion (I/R) injury. (elsevierpure.com)
  • Cardiac I/R induced a marked inhibition of cardiac function and myocardial injury. (phoenixpeptide.com)
  • these socalled pleiotropic properties include anti-inflammatory effects, plaque stabilization, improved endothelial function and inhibition of vascular smooth muscle cell proliferation. (ac.ir)
  • Inhibition of the mitochondrial fission protein dynamin-related protein 1 improves survival in a murine cardiac arrest model. (uchicago.edu)
  • More importantly, this study revealed that pharmacological PDE1 inhibition attenuated the progression of pre-established AAA. (rochester.edu)
Therapeutic6
  • However, mitigation strategies to preserve cardiac function after an ischemic event have often only focused on individual therapeutic agents, and the results have not been ideal. (prohealth.com)
  • The first original paper this week suggests that targeting fibronectin polymerization may be a new therapeutic strategy for treating cardiac fibrosis. (libsyn.com)
  • In summary, interfering with fibronectin polymerization may be a new therapeutic strategy for treating cardiac fibrosis and heart failure. (libsyn.com)
  • In this review, we discuss the differentiation and paracrine functions of ADSCs, the strategies promoting their therapeutic efficacy, and their clinical usage. (biomedcentral.com)
  • Accordingly, mechanism of enhancing myocardial energetic efficiency by stimulating glucose availability and utilization has led to the vigorous pursuit of therapeutic approaches designed to augment glucose uptake and oxidation. (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)
Cardioprotection6
  • Heusch G: Myocardial ischaemia-reperfusion injury and cardioprotection in perspective. (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)
  • 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)
  • The present study therefore provided novel evidence that DJ‑1 is involved in the delayed cardioprotection of IPC against I/R injury in vivo. (spandidos-publications.com)
  • Our previous study revealed that hypoxia preconditioning of H9c2 cardiomyocytes significantly increased the de novo synthesis of DJ-1 and induced cardioprotection against prolonged hypoxic injury 24 h later ( 17 ). (spandidos-publications.com)
  • One such area of interest is the ability to modulate myocardial glucose uptake and its impact on cardioprotection. (biomedcentral.com)
Infarct5
  • METHODS AND RESULTS: In 2 mouse models, MAP-1 preserves cardiac function, decreases infarct size, decreases C3 deposition, inhibits MBL deposition, and prevents thrombogenesis. (regionh.dk)
  • Thus, we hypothesized that the endogenous mannose-binding lectin (MBL)/ficolin-associated protein-1 (MAP-1) that inhibits complement activation in vitro also could be an in vivo regulator by attenuating myocardial schema/reperfusion injury and thrombogenesis when used at pharmacological doses in wild-type mice.METHODS AND RESULTS: In 2 mouse models, MAP-1 preserves cardiac function, decreases infarct size, decreases C3 deposition, inhibits MBL deposition, and prevents thrombogenesis. (regionh.dk)
  • 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)
  • Lactate dehydrogenase (LDH) and creatine kinase‑MB (CK‑MB) release, infarct size, cardiac function, superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx) activities, malondialdehyde (MDA), intracellular reactive oxygen species (ROS), and DJ‑1 protein expression levels were assessed. (spandidos-publications.com)
  • In addition, IPC reduced LDH and CK‑MB release, attenuated myocardial infarct size, improved cardiac function following I/R, and inhibited the elevation of ROS and MDA and the decrease in activities of the antioxidant enzymes SOD, CAT and GPx. (spandidos-publications.com)
Troponin1
  • The expression levels of the myocardial injury marker cardiac troponin I (CTNI) in serum were tested at 6 hours after CPR or TMZ + CPR. (dirjournal.org)
Myocytes1
  • 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)
Cardioprotective effects3
  • Research done in animals shows that treatment with NAD+ precursors like NMN have cardioprotective effects against ischemia/reperfusion injury (4). (prohealth.com)
  • These results suggest that IMD(1-53), like adrenomedullin, has cardioprotective effects against myocardial I/R injury. (phoenixpeptide.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)
Release of myocardial2
  • 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)
  • The release of myocardial protein and lactate dehydrogenase (LDH) and the formation of malondialdehyde (MDA) were assayed. (phoenixpeptide.com)
Morbidity and morta1
  • Cardiac complications constitute a major cause of postoperative morbidity and mortality in surgical patients. (medscape.com)
Rats4
  • These results showed that mangiferin could ameliorate cardiac fibrosis in D-galactose-induced aging rats possibly via inhibiting TGF-β/p38/MK2 signaling pathway. (kjpp.net)
  • This study aimed to evaluate the effects of TQ on spatial memory and hippocampal long-term potentiation (LTP) in rats with thioacetamide (TAA)-induced liver injury and hepatic encephalopathy. (magiran.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)
  • The number and function of circulating endothelial progenitor cells (EPCs) were increased in PEMF treating rats. (pemfglobal.com)
Significantly6
  • 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)
  • Reperfusion with IMD(1-53) significantly ameliorated the inhibited cardiac function and bradycardia induced by I/R. Compared with the I/R-treatment alone, IMD(1-53) reperfusion augmented CPF, LVSP, and maximal rate of increase and decrease of left ventricle pressure (+/-LVdP/dt(max)) and decreased LVDP. (phoenixpeptide.com)
  • Reperfusion with IMD significantly attenuated the I/R injury. (phoenixpeptide.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)
  • The in vivo results showed that per-treatment of PEMF could significantly improve the cardiac function in I/R injury group. (pemfglobal.com)
  • Importantly, VSIG4 is significantly reduced after myocardial ischemia-reperfusion injury in patients undergoing coronary artery bypass grafting [ 11 ]. (thno.org)
Hypoxia1
  • 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)
Cardiomyocytes4
  • 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)
  • Here, we describe the regeneration of left ventricular (LV) wall using decellularized whole rabbit heart scaffolds recellularized exclusively with human induced pluripotent stem cell-derived endothelial cells, cardiomyocytes, and other cardiac cell types. (bvsalud.org)
  • These results demonstrate the ability to tissue engineer a vascularized, full-thickness LV wall with an unparalleled level of microanatomical organization and multicellular composition, using decellularized ECM and human cardiomyocytes, endothelial cells, and other cardiac cell types. (bvsalud.org)
  • Numerous apoptotic cardiomyocytes were found in ischemic fields in ischemia-reperfusion groups and werent observed in the sham-operated group. (ac.ir)
Protective6
  • Protective effects of intermedin/adrenomedullin2 on ischemia/reperfusion injury in isolated rat hearts. (phoenixpeptide.com)
  • The present study was designed to determine the protective effect of IMD on cardiac ischemia/reperfusion (I/R) injury and its possible mechanism. (phoenixpeptide.com)
  • Interestingly, the above IMD effects were similar to those of adrenomedullin (10(-8)mol/L). These results suggest that IMD, like adrenomedullin, exerts cardio-protective effects against myocardial I/R injury. (phoenixpeptide.com)
  • The goal of this proposal is to investigate a novel preservation method utilizing hydrogen sulfide (H2S) to induce a protective state of hibernation against I/R injury. (gotomydoctor.com)
  • Inflammation is a protective physiological response of an organism to chemical, physical, infectious agents, environmental toxins, ischemia or an antigen-antibody interaction. (biomedcentral.com)
  • This study aimed to determine the potential myocardial protective effect and possible mechanism of action of D. odorifera essential oil (DOEO). (wjtcm.net)
Contributes2
  • Lysosomes play a pivotal role in the inflammation process, and PGRN is one of the key regulators in their functioning, which contributes to the immunomodulatory mechanism in the pathogenesis of CVDs. (biomedcentral.com)
  • It was shown that functional Fas system contributes to apoptotic myocardial cell death in response to ischemia/reperfusion injury [ 4 , 5 ]. (ac.ir)
Vitro2
  • Thus, we hypothesized that the endogenous mannose-binding lectin (MBL)/ficolin-associated protein-1 (MAP-1) that inhibits complement activation in vitro also could be an in vivo regulator by attenuating myocardial schema/reperfusion injury and thrombogenesis when used at pharmacological doses in wild-type mice. (regionh.dk)
  • 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)
Pathological2
  • Using mouse and human cardiac myofibroblasts, authors found that the fibronectin polymerization inhibitor pUR4 attenuated the pathological phenotype exhibited by mouse and human myofibroblasts by decreasing fibronectin polymerization and collagen deposition into the extracellular matrix as well as by myofibroblast proliferation and migration. (libsyn.com)
  • These pathological features were previously linked to aberrant expression and remodeling of the cardiac gap junction protein connexin43 (Cx43). (jci.org)
Isoproterenol4
  • In this paper from co-first authors Dr Park and Ranjbarvaziri, corresponding author Dr Ardehali, from David Geffen School of Medicine, University of California, Los Angeles, the authors utilized a novel multiple-strain approach known as the Hybrid Mouse Diversity Panel to characterize the contributions of cardiac fibroblasts to the formation of isoproterenol-induced cardiac fibrosis in three strains of mice. (libsyn.com)
  • They found that isolated cardiac fibroblasts treated with isoproterenol exhibited strain-specific increases in the levels of activation, but showed comparable levels of proliferation. (libsyn.com)
  • Similar results were found in vivo with fibroblast activation but not proliferation correlating with the differential levels of cardiac fibrosis after isoproterenol treatment. (libsyn.com)
  • RNA sequencing revealed that cardiac fibroblasts from each strain exhibited unique gene expression changes in response to isoproterenol. (libsyn.com)
Mesenchymal stem2
  • 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)
  • Our investigation indicates that most of these studies examined endothelial progenitor cells, hematopoietic stem cells, mesenchymal stem cells, adipose-derived stem cells, and a few others were about less-discussed types of stem cells such as cardiac stem cells, myeloblasts, and induced pluripotent stem cells. (magiran.com)
Fibrosis6
  • Cardiac fibrosis is a pathophysiological process of cardiac aging. (kjpp.net)
  • In this study, rat model of cardiac fibrosis was induced by injected with 150 mg/kg/d Dgalactose for 8 weeks. (kjpp.net)
  • Cardiac fibrosis was evaluated by observing collagen deposition via masson and sirius red staining, as well as by examining the expression of extracellular matrix proteins via Western blot analysis. (kjpp.net)
  • 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)
  • The next study highlights the importance of genetic variation in cardiac fibrosis and suggests that while fibroblast activation is a response that parallels the extent of scar formation, proliferation may not necessarily correlate with levels of fibrosis. (libsyn.com)
  • Therefore, modulating the level of myocardial fibrosis after AMI is important for delaying or reversing VR. (thno.org)
Intracellular calcium1
Cytokines2
  • LPS results in the overexpression and release of proinflammatory cytokines, including tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and interleukin-6 (IL-6), which contribute to LPS-induced multiple organs failure including myocardial depression [ 6 , 7 ]. (biomedcentral.com)
  • 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)
Mechanisms3
  • 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)
  • In the present study, we investigated for the first time whether PEMF treatment could improve the myocardial ischaemia/reperfusion (I/R) injury and uncovered its underlying mechanisms. (pemfglobal.com)
Murine1
Fibroblasts1
  • We also determined the function of cardiac fibroblasts (CFs) through gain- or loss-of-function experiments. (thno.org)
Lactate dehydrogenase3
Vivo1
  • However, whether the increase in DJ-1 expression mediates protection against ischemia/reperfusion (I/R) injury in vivo during the late phase of IPC remains to be determined. (spandidos-publications.com)
Biomarkers2
  • Machine-learning to stratify diabetic patients using novel cardiac biomarkers and integrative genomics. (wvu.edu)
  • Cardiac biomarkers Acute coronary syndromes result from acute obstruction of a coronary artery. (msdmanuals.com)
Ventricular1
  • Meanwhile, the myocardial injury marker CTNI was upregulated considerably ( P = 0.014, P = 0.021), and the left ventricular function of the animal heart also markedly deteriorated with the downregulation of ATP after CPR. (dirjournal.org)
Protects1
  • Moreover, it was observed that, PGRN protects the heart against ischemia-reperfusion injury. (biomedcentral.com)
Pathophysiology1
  • We have recently shown that the lectin pathway-specific carbohydrate recognition subcomponent mannose-binding lectin plays an essential role in the pathophysiology of thrombosis and ischemia/reperfusion injury. (regionh.dk)
Oxidation1
Heart16
  • 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)
  • What Happens During a Heart Attack and Reperfusion Injury? (prohealth.com)
  • During myocardial ischemia (lack of blood flow to the muscle tissue of the heart, commonly referred to as a "heart attack"), blood flow is interrupted because of damage to one or more of the coronary blood vessels that irrigate the heart. (prohealth.com)
  • Reperfusion injury increases the damage done after events such as heart attacks. (prohealth.com)
  • In many cases, damage to heart tissue by reperfusion injury is greater than the damage done by the interruption of blood flow. (prohealth.com)
  • The age-related cardiac decline was estimated by detecting the relative weight of heart, the serum levels of cardiac injury indicators and the expression of hypertrophic biomakers. (kjpp.net)
  • Although a recent joint society scientific statement (the American Association of Cardiovascular Pulmonary Rehabilitation, the American Heart Association, and the American College of Cardiology) suggests home-based cardiac rehab (CR) is appropriate for low- and moderate-risk patients, there are no paradigms to define such individuals with coronary heart disease. (journaltocs.ac.uk)
  • In still other cells connexons have been shown to occur in mitochondrial membranes and appear to play a role in heart ischaemia. (wikipedia.org)
  • We hypothesized that the donor heart preservation with hypoxic conditioned medium derived from BMSCs (CM-BMSCs) would improve post-transplant graft function. (researchsquare.com)
  • Therefore, attenuating myocardial I/R injury during the heart transplant procedure would have a favorable impact on improving short- and long-term graft function and recipient's survival(6). (researchsquare.com)
  • Dr. Chen's researches have been focused on cardiovascular diseases from development, adult heart remodeling and cardiac regeneration. (z2hospital.com)
  • The extent of reperfusion injury is directly proportional to preservation time in cold storage, and research has shown that with static storage methods, heart storage time will not exceed six hours. (gotomydoctor.com)
  • Additionally, machine reperfusion induces the production of ROS, which results in I/R injury to the heart. (gotomydoctor.com)
  • In addition, it has been shown that atorvastatin can protect the isolated mouse heart against reperfusion-induced injury [ 6 ]. (ac.ir)
  • Clinically, beneficial effects of GLP-1 have also been demonstrated in patients with myocardial ischemia and heart failure. (biomedcentral.com)
  • 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)
Diabetic1
  • Over 15 randomized clinical studies have shown that intravenous administration of 300-600 mg of lipoic acid a day greatly improves nerve function and relieves pain symptoms in diabetic neuropathy patients. (lifeextension.com)
Endogenous1
  • 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)
Anti-inflammatory effects1
  • Background Dexmedetomidine has been shown to confer direct renoprotection by stabilizing the sympathetic system, exerting anti-inflammatory effects and attenuating ischemia/reperfusion (I/R) injury in preclinical studies. (medscape.com)
Nrf21
  • 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)
Diastolic1
  • Transfer of this segment of chromosome 8 from the BN-Lx strain onto the SHR background resulted in substantial reductions in systolic and diastolic blood pressure and cardiac mass. (jci.org)
Cardiovascular diseases2
  • Especially, Dr. Chen would like, but not limited, to elucidate how noncoding RNA regulates cardiac hypertrophy and cardiac regeneration during the cardiovascular diseases. (z2hospital.com)
  • Dr. Chen's team use cardiac cell system, mouse genetic model and AAV system to study the cardiovascular diseases. (z2hospital.com)
Patients7
  • Multiple alterations in serum thyroid function test findings have been recognized in patients with a wide variety of NTIs without evidence of preexisting thyroid or hypothalamic-pituitary disease. (medscape.com)
  • A general conviction exists that patients with thyroid function test result abnormalities do not have hypothyroidism despite the low serum hormone levels in blood and low T3 in most of the tissues. (medscape.com)
  • Lipopolysaccharide (LPS), a bacterial endotoxin located in the outer membrane of the cell wall of the Gram-negative bacteria, is considered as the principal factor responsible for multiple organs damage including myocardial injury in patients with sepsis [ 2 , 3 ]. (biomedcentral.com)
  • Infection is the leading cause of death and prolonged hospitalization in severely burned patients that survive the acute phase of injury. (vumc.org)
  • Methods We searched EMBASE, PubMed, and Cochrane CENTRAL databases for randomized controlled trials (RCTs) comparing the renal effect of dexmedetomidine versus placebo or other anesthetic drugs in adult patients undergoing cardiac surgery. (medscape.com)
  • Conclusions Perioperative administration of dexmedetomidine in adult patients undergoing cardiac surgery may reduce the incidence of postoperative AKI. (medscape.com)
  • Future trials are needed to determine the dose and timing of dexmedetomidine in improving outcomes, especially in patients with decreased baseline kidney function. (medscape.com)
Endothelial1
  • Here, we successfully revascularized and repopulated a large, full-thickness portion of a ventricle using human induced pluripotent stem cell-derived endothelial and cardiac cells. (bvsalud.org)
Coronary artery1
  • 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)
Proinflammatory1
  • 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)
Bone marrow-derived1
  • Given these advantages, ADSCs may be better candidates for myocardial regeneration than bone marrow-derived stem cells. (biomedcentral.com)
Clinical2
  • Previous studies have shown that ischemia/reperfusion (I/R) injury acts as a significant role in PGD(4), contributing to adverse short- and long-term clinical outcomes in the recipients. (researchsquare.com)
  • Results from clinical trials of dexmedetomidine on acute kidney injury (AKI) following adult cardiac surgery are controversial. (medscape.com)
Arrest3
  • Suppression of Superoxide-Hydrogen Peroxide Production at Site IQ of Mitochondrial Complex I Attenuates Myocardial Stunning and Improves Postcardiac Arrest Outcomes. (uchicago.edu)
  • Cardiac Arrest Cardiac arrest is the cessation of cardiac mechanical activity resulting in the absence of circulating blood flow. (msdmanuals.com)
  • Cardiac arrest stops blood from flowing to vital organs, depriving them of. (msdmanuals.com)
Inflammatory response1
  • We showed that VSIG4 promotes scar formation and orchestrates the myocardial inflammatory response after AMI, while also promoting TGF-β1 and IL-10. (thno.org)
Pathways1
  • Recent studies have identified HDLs (high-density lipoproteins) as a potential candidate for mitigating coronary ischemia/reperfusion injury via a broad spectrum of signaling pathways. (unipr.it)
Mitochondrial function1
  • As a graduate student, Brandon developed and pioneered an optogenetic approach to control mitochondrial function using light. (rochester.edu)
Methods3
  • 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)
  • Current methods of cold static storage have reached their limits in storage time due to the extent of ischemia-reperfusion (I/R) injury induced during static cold storage. (gotomydoctor.com)
  • [ 3 , 4 ] Further refinements in CPB hardware and techniques, perfusion methods, myocardial and brain protection over the past 2 decades contributed to improved outcomes of surgical treatment of CHD. (medscape.com)
Hydrogen1