AnatomyOrganismsDiseasesChemicals and DrugsAnalytical, Diagnostic and Therapeutic Techniques and EquipmentPhenomena and ProcessesDisciplines and OccupationsHealth Care
Myocardial Reperfusion InjuryReperfusion InjuryMyocardial IschemiaMyocardial ReperfusionMyocardiumIschemic PostconditioningIschemic Preconditioning, MyocardialCardiotonic AgentsMyocardial InfarctionMyocytes, CardiacReperfusionRats, Sprague-DawleyIschemiaCreatine KinaseDisease Models, AnimalHeartPeroxidaseVentricular Function, LeftL-Lactate DehydrogenaseApoptosisReceptor, Adenosine A3Rats, WistarMitochondria, HeartHeart Function TestsMice, Inbred C57BLHemodynamicsTime FactorsCoronary CirculationMyocardial ContractionMice, KnockoutIschemic PreconditioningOxidative StressBrain IschemiaSignal TransductionNitric OxideProto-Oncogene Proteins c-aktNitric Oxide Synthase Type IINitric Oxide Synthase Type IIIElectrocardiographyCoronary VesselsDogsWarm IschemiaPerfusionNecrosisProtective AgentsNeutrophilsCardioplegic SolutionsRabbitsMalondialdehydeRandom AllocationArrhythmias, CardiacSwineCold IschemiaPeroxynitrous AcidThrombectomyReactive Oxygen SpeciesAntioxidantsTroponin IHeart Arrest, InducedCyclic S-OxidesWounds and InjuriesAngioplasty, Balloon, CoronaryCoronary AngiographySuctionCaspase 3KidneyKATP ChannelsNeutrophil InfiltrationCoronary DiseaseHeart RateHeart VentriclesCytoprotectionMicrocirculationLiverP-SelectinEnzyme InhibitorsBlotting, WesternIn Situ Nick-End LabelingBlood PressureCreatine Kinase, MB FormAcute Kidney InjuryMitochondrial Membrane Transport ProteinsConstrictionCells, CulturedTumor Necrosis Factor-alphaEndothelium, VascularModels, AnimalThrombolytic TherapySuperoxide DismutaseOrgan PreservationTreatment OutcomeAspartate AminotransferasesOrgan Preservation SolutionsNeuroprotective AgentsAlanine TransaminaseMyocardial StunningInfarction, Middle Cerebral ArteryHeme Oxygenase-1EchocardiographyMice, Transgenic
InfarctionOxidative stressApoptosisInhibitionDysfunctionMyocardiumTroponinAcuteCoronaryCardioprotectionRelease of myocardialHypoxiaVitroGlobal ischemiaCardiomyocytesInhibitorCardioprotectiveSignificantlyMesenchymal stemPost-ischemic cardiacProtective effectMechanismsMurineFibrosisInflammatory responsesInfarct sizeHypertrophyEnergy substratesMorbidity and mortaRenalExperimentalPathophysiologyProtectsInnate immunityNecrosisHeartProinflammatoryCardiomyocyteClinicalSubsequentPathogenesisMiceFunctionLactate dehydrogenaseArrestMethodsHydrogenRatsCardiopulmonaryTissuesProteinDepositionModel
Infarction28
Oxidative stress12
Apoptosis10
  • Reports showed that mangiferin administration ameliorated isoproterenol-induced apoptosis [ 12 ] and hydrogen peroxide-induced cell injury [ 10 ] in cardiomyocytes. (kjpp.net)
  • In conclusion, the present study demonstrated that SA inhibits the apoptosis of H9c2 cardiomyocytes following H/R injury via reduced activation of the p38MAPK and JNK signaling pathways. (spandidos-publications.com)
  • The underlying mechanisms behind myocardial I/R injury are associated with a number of factors, including substantial free radical production, intracellular calcium overload, increased inflammation, myocardial necrosis and apoptosis ( 6 ). (spandidos-publications.com)
  • The results demonstrated that SA inhibited apoptosis signaling in H9c2 cardiomyocytes via downregulation of p38 mitogen-activated protein kinase (p38MAPK) and c-Jun N-terminal kinase (JNK) signaling pathways following hypoxia/reoxygenation (H/R) injury. (spandidos-publications.com)
  • 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)
  • End of the experiments we collected blood samples for the measurement of endothelial dysfunction parameter asymmetric dimethylarginine (ADMA), apoptosis parameters M30 and M65, cardiac risk factors homocysteine and serum lipid profile.CDP-choline treatment significantly attenuated the size of infarct area induced by long term ischemia-reperfusion versus saline group. (uludag.edu.tr)
  • Furthermore, ADSCs secrete a series of paracrine factors to promote neovascularization, reduce apoptosis, and inhibit fibrosis, which contributes to cardiac regeneration. (biomedcentral.com)
Inhibition4
  • 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)
  • We aim to attenuate this inflammation by therapeutic inhibition. (ncrg.no)
  • The projects within this topic aim to resolve this challenge by significantly reducing tissue injury in the course of I/R using a novel and groundbreaking therapy of double inhibition of the innate immune system, namely the complement system and the toll-like receptors (TLR). (ncrg.no)
Dysfunction11
  • 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)
  • Diabetic cardiomyopathy is defined as a ventricular dysfunction initiated by alterations in cardiac energy substrates in the absence of coronary artery disease and hypertension. (hindawi.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)
  • There is substantial evidence that endothelial injury during organ procurement and preservation, caused by ischemia and subsequent reperfusion, results in endothelial dysfunction. (frontierspartnerships.org)
  • Myocardial stunning is a postischemic reversible contractile dysfunction of the heart. (nii.ac.jp)
  • 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)
  • 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)
Myocardium7
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)
Acute4
  • Exogenous cell-based therapy has emerged as a promising new strategy to facilitate repair of hearts damaged by acute or chronic injury. (bvsalud.org)
  • Infection is the leading cause of death and prolonged hospitalization in severely burned patients that survive the acute phase of injury. (vumc.org)
  • Cardiac biomarkers Acute coronary syndromes result from acute obstruction of a coronary artery. (msdmanuals.com)
  • Results from clinical trials of dexmedetomidine on acute kidney injury (AKI) following adult cardiac surgery are controversial. (medscape.com)
Coronary7
  • 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)
  • 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)
  • in 1971 [ 2 ], diabetic cardiomyopathy (DCM) is characterized by the direct effect of diabetes on cardiac structure and function in the absence of coronary artery disease, hypertension, or other cardiac pathologies. (hindawi.com)
  • 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 this study, we investigated that if CDP-choline has protective effects against long-term myocardial ischemia-reperfursion injury in rats.Long term ischemia-reperfusion was produced in anaesthetized rats by ligature of the left main coronary artery for 30 minutes followed by reperfusion period for the next 180 minutes. (uludag.edu.tr)
  • 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)
  • DCM is a cardiac pathological condition in patients with DM characterized by the appearance of aberrant myocardial morphology and cardiac functions in the truancy of other factors, such as coronary artery disease, hypertension, and prominent valvular disease [ 3 ] . (encyclopedia.pub)
Cardioprotection2
  • Heusch G: Myocardial ischaemia-reperfusion injury and cardioprotection in perspective. (spandidos-publications.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)
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)
Hypoxia4
  • 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)
  • 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)
  • Myocardial ischemia, also called cardiac ischemia or hypoxia/reoxygenation (H/R)-induced heart damage, is caused by decreased blood flow [ 1 ]. (biomedcentral.com)
  • My group has developed unique models of hypoxia/reoxygenation of cultured endothelial cells in combination with a full blood model and the use of ex vivo machine perfusion to simulate reperfusion in porcine kidneys, porcine and human livers. (ncrg.no)
Vitro6
  • The present study aimed to clarify the cardioprotective effect of SA in myocardial I/R injury in vitro and explore the potential molecular mechanisms. (spandidos-publications.com)
  • The functional recovery from 30-min global ischemia was studied in the isolated hearts perfused in-vitro. (nii.ac.jp)
  • 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)
  • 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)
  • To investigate this hypothesis, the H9c2 cardiomyocyte cell line was used to establish an in vitro myocardial H/R injury model to explore the roles and potential mechanisms of STA in myocardial H/R injury. (biomedcentral.com)
  • My overall research aim is (1) to describe innate immunity mechanisms in ischemia/reperfusion injury and (2) to attenuate the reperfusion injury both in vitro and in vivo with high potential for transfer to clinical studies. (ncrg.no)
Global ischemia1
Cardiomyocytes6
  • 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)
  • 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)
  • Therefore, the study aimed to investigate the protective effects and mechanisms of STA on H/R injury of cardiomyocytes. (biomedcentral.com)
  • However, the role of STA on the H/R injury of cardiomyocytes through the SIRT1-Nrf2 pathway remains unexplored. (biomedcentral.com)
Inhibitor2
  • 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)
  • We hypothesized that overexpression of calpastatin, an endogenous calpain inhibitor, would attenuate the ischemia/reperfusion injury in the heart. (nii.ac.jp)
Cardioprotective3
  • Research done in animals shows that treatment with NAD+ precursors like NMN have cardioprotective effects against ischemia/reperfusion injury (4). (prohealth.com)
  • Although, CDP-choline treatment did not significantly alter the blood levels of any parameter (ADMA, M30, M65, homocysteine, serum lipid profile).Results of this study show that CDP-choline exerts cardioprotective effects in long term myocardial ischemia-reperfusion injury. (uludag.edu.tr)
  • These results suggest that IMD(1-53), like adrenomedullin, has cardioprotective effects against myocardial I/R injury. (phoenixpeptide.com)
Significantly5
  • 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)
  • Aromatase metabolizes testosterone to 17b- estradiol (E2) and thereby significantly contributes The volatile anesthetic desflurane (DES) effectively reduces cardiac infarct size following experimental ischemia/reperfusion injury in the mouse heart. (uni-wuerzburg.de)
  • The recovery of left ventricular developed pressure, max dP/dt, and min dP/dt during 60-min reperfusion was significantly greater in the calpastatin transfected group than control group heart by gene transfer. (nii.ac.jp)
  • 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)
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)
Post-ischemic cardiac1
  • 2. PI3K p85 and Bcl-2 are targets of miR-503, and the post-ischemic cardiac PI3K p85 protein level is decreased in vivo. (fullpicture.app)
Protective effect3
  • Cytidine diphosphocholine (CDP-choline) is in use for treatments of stroke and head trauma in Japan and several European countries for many years because of its protective effect against cerebral injury. (uludag.edu.tr)
  • Stachydrine (STA), an active constituent of Leonurus heterophyllus sweet, could have a protective effect on myocardial H/R injury, which remains unexplored. (biomedcentral.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)
Mechanisms3
  • 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)
  • Therefore, exploring new therapeutic agents and investigating their potential mechanisms underlying myocardial H/R injury is important. (biomedcentral.com)
  • However, the effects and the detailed mechanisms of STA in myocardial H/R injury are unknown. (biomedcentral.com)
Murine2
Fibrosis12
  • 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)
  • 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)
  • The first original paper this week suggests that targeting fibronectin polymerization may be a new therapeutic strategy for treating cardiac fibrosis. (libsyn.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 summary, interfering with fibronectin polymerization may be a new therapeutic strategy for treating cardiac fibrosis and heart failure. (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)
  • 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)
  • 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)
  • Chronic allograft injury (CAI), consisting of vasculopathy and interstitial fibrosis, affects approximately 50% of patients after 10 years and limits long-term survival following heart transplantation ( 1 ). (frontierspartnerships.org)
  • Recent studies have demonstrated that supplementation of nitric oxide (NO), or increased expression of endothelial NO-synthase (eNOS) protects against both IR-injury and fibrosis ( 5 , 6 ). (frontierspartnerships.org)
Inflammatory responses1
  • 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)
Infarct size3
  • The volatile anesthetic desflurane (DES) effectively reduces cardiac infarct size following experimental ischemia/reperfusion injury in the mouse heart. (uni-wuerzburg.de)
  • Anastrozole blocked DES induced preconditioning and increased infarct size compared to DES alone (37.94615.5% vs. 17.163.62%) without affecting area at risk and systemic hemodynamic parameters following ischemia/reperfusion. (uni-wuerzburg.de)
  • 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)
Hypertrophy1
  • 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)
Energy substrates1
  • Glucose and fatty acids are important energy substrates for myocardial metabolism. (dirjournal.org)
Morbidity and morta2
  • Cardiac complications are the leading cause of morbidity and mortality in diabetic patients [ 1 ]. (hindawi.com)
  • Cardiac complications constitute a major cause of postoperative morbidity and mortality in surgical patients. (medscape.com)
Renal3
  • has been demonstrated to attenuate renal ischemia‑reperfusion (I/R) injury. (spandidos-publications.com)
  • SA also attenuated renal I/R injury ( 11 ). (spandidos-publications.com)
  • 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)
Experimental1
  • 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)
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)
Protects1
  • Moreover, it was observed that, PGRN protects the heart against ischemia-reperfusion injury. (biomedcentral.com)
Innate immunity1
  • Focus: Innate immunity in ischemia/reperfusion injury - transfer to the clinic. (ncrg.no)
Necrosis1
  • 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)
Heart14
  • 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)
  • 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)
  • 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)
  • In still other cells connexons have been shown to occur in mitochondrial membranes and appear to play a role in heart ischaemia. (wikipedia.org)
  • Cold ischemia and subsequent reperfusion injury are non-immunologic cornerstones in the development of graft injury after heart transplantation. (frontierspartnerships.org)
  • Dr. Chen's researches have been focused on cardiovascular diseases from development, adult heart remodeling and cardiac regeneration. (z2hospital.com)
  • Adenovirus-mediated overexpression of calpastatin could be a novel biological storage to improve heart transplantation by minimizing ischemia/reperfusion injury. (nii.ac.jp)
  • 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)
  • 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)
  • 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)
Proinflammatory2
  • 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)
Cardiomyocyte2
  • 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)
  • Cells were pretreated with STA (50 µM) 2 h before H/R. Cardiomyocyte injury was evaluated by CCK-8 assay and lactate dehydrogenase (LDH) release. (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)
  • Therefore, it is crucial in the clinical setting to detect myocardial metabolism conditions in real-time to evaluate the latent cardiac injury and make optimum treatment plans during the ROSC. (dirjournal.org)
Subsequent2
  • 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)
  • 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)
Pathogenesis1
  • 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)
Mice3
  • CR-PSMI in intact mice was achieved by transgenic (tg) overexpression of a peptidase-disabled mouse β5 subunit (T60A-β5) driven by an attenuated mouse mhc6 promoter. (elsevierpure.com)
  • A new mouse cardiac electrophysiology method was used to study mice harboring an alpha-myosin heavy chain Arg403Gln missense mutation (alpha-MHC403/+), which results in histological and hemodynamic abnormalities characteristic of familial hypertrophic cardiomyopathy (FHC) and sudden death of uncertain etiology during exercise. (jci.org)
  • Priming with Toll-like receptor 4 agonists have been shown to augment neutrophil antimicrobial responses and enhance resistance against infection after severe burn injury in mice. (vumc.org)
Function6
  • 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)
  • In contrast, myocardial injury and cardiac function were greatly improved with the increase of ATP in the CPR + TMZ group. (dirjournal.org)
  • 18 F) FDG PET/CT, as a non-invasive technology, can monitor myocardial energy metabolism and cardiac function by tracking changes in glucose metabolism after CPR. (dirjournal.org)
  • Effects of intermedin(1-53) on cardiac function and ischemia/reperfusion injury in isolated rat hearts. (phoenixpeptide.com)
  • The present study was designed to observe the effects of IMD(1-53) on cardiac function in ischemia/reperfusion (I/R) injury in isolated rat hearts. (phoenixpeptide.com)
  • Cardiac function was measured. (phoenixpeptide.com)
Lactate dehydrogenase1
Arrest2
  • 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)
Methods2
  • 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)
Hydrogen2
  • In this study, we demonstrate that MnSOD is down-regulated upon hydrogen peroxide treatment or ischemia/reperfusion (I/R) injury. (molcells.org)
  • 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)
Rats1
  • 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)
Cardiopulmonary1
  • Impaired energy metabolism was closely related to myocardial damage after cardiopulmonary resuscitation (CPR). (dirjournal.org)
Tissues1
Protein1
  • In addition, perfusion with IMD markedly attenuated the leakage of LDH, total protein and myoglobin from myocardia compared with I/R alone. (phoenixpeptide.com)
Deposition1
  • Fibronectin polymerization is necessary for collagen matrix deposition and is a key contributor to increased abundance of cardiac myofibroblast following cardiac injury. (libsyn.com)
Model1
  • Dr. Chen's team use cardiac cell system, mouse genetic model and AAV system to study the cardiovascular diseases. (z2hospital.com)