• 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)
  • Restoration of blood supply, termed reperfusion, has been used to treat ischemic myocardium and prevent further tissue damage. (spandidos-publications.com)
  • Both ischemic and reperfused rat myocardium can undergo apoptotic cell death, however the myocardium, which is subjected to ischemia followed by reperfusion, undergoes accelerated apoptosis [ 3 ]. (ac.ir)
  • These pleiotropic effects thus have a major role in protecting the myocardium against ischemic injury. (ac.ir)
  • However, whether GRh2 has a protective effect on ischaemia/reperfusion (I/R) in the myocardium has yet to be elucidated. (spandidos-publications.com)
  • The present study aimed to identify the anti‑inflammatory and antioxidant effects of GRh2 on I/R in the myocardium and its underlying mechanism. (spandidos-publications.com)
  • In the ischemic myocardium, an increase in glucose uptake and subsequent ATP generated through glycolysis helps to sustain myocardial electric and mechanical performance, maintains cellular ultrastructure, promotes myocardial recovery. (biomedcentral.com)
  • The injured myocardium develops an evolving dependence on glucose as its preferred metabolic substrate while development of myocardial insulin resistance is associated with the progression of heart failure and increased incidence as well as severity of the damaged hearts. (biomedcentral.com)
  • 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)
  • 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)
  • NEW & NOTEWORTHY Remote ischemic conditioning (RIC) and long-term glyceryl trinitrate (GTN) treatment protect against ischemia-reperfusion injury in both human endothelium and rat myocardium. (ox.ac.uk)
  • 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)
  • Thus, inhibition of oxidative stress and myocardial apoptosis is beneficial in the treatment of myocardial I/R injury. (spandidos-publications.com)
  • 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)
  • The resulted data showed that curcumin alleviates myocardial inflammatory responses and oxidative stress during myocardial IRI. (edu.iq)
  • 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)
  • 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)
  • 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)
  • 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)
  • 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)
  • Compared to rats, AGS display robust myocardial ischemic tolerance following DHCA (both reduced myocardial necrosis and apoptosis). (duke.edu)
  • Upregulation of Fas expression in myocardial ischemia-reperfusion can induce cardiomyocyte apoptosis, and atorvastatin can significantly inhibit cardiomyocyte apoptosis by inhibiting Fas expression. (ac.ir)
  • Apoptosis of the cardiomyocytes has been demonstrated in animal models with coronary artery occlusion [ 1 ], and experimental evidence suggests that myocardial cells are able to undergo apoptosis during ischemia followed by reperfusion [ 2 ]. (ac.ir)
  • Reports showed that mangiferin administration ameliorated isoproterenol-induced apoptosis [ 12 ] and hydrogen peroxide-induced cell injury [ 10 ] in cardiomyocytes. (kjpp.net)
  • Res effectively suppress the cardiomyocytes hypertrophy and apoptosis induced by ISO, characterized by the reduction of the myocardial cell surface area, the ANP gene expression, the LDH and MDA leakage amount and the rate of cell apoptosis, while decrease of the protein expression of GRP78, GRP94 and CHOP, and reverse the expression of Bcl-2 and Bax. (karger.com)
  • In summary, Res treatment effectively suppressed myocardial hypertrophy and apoptosis at least partially via inhibiting ER stress. (karger.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)
  • All of these factors are known to result in myocardial apoptosis(5) and the acceleration of allograft rejection or chronic allograft dysfunction. (researchsquare.com)
  • Elucidating the molecular mechanisms of cardiomyocyte apoptosis would be of great importance for tackling apoptosis related heart disease. (molcells.org)
  • 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)
  • 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)
  • 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)
  • 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 I/R induced a marked inhibition of cardiac function and myocardial injury. (phoenixpeptide.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)
  • The in vivo results showed that per-treatment of PEMF could significantly improve the cardiac function in I/R injury group. (pemfglobal.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)
  • It is important to understand how these mechanisms are dynamically regulated by pivotal molecular targets and potentially reversed in the context of cardioprotection [ 6 ]. (hindawi.com)
  • The lack of effective treatments to reduce the consequences of myocardial ischemia-reperfusion injury and the increased reliance on percutaneous and surgical treatments for coronary and valvular disease or end-stage heart failure make it critically important to identify new targets and strategies for cardioprotection. (duke.edu)
  • Using a clinically relevant model of surgical deep hypothermic circulatory arrest (DHCA) combined with targeted metabolomic and proteomic profiling, we are investigating how changes in hibernation-specific myocardial expression/activity of PPARα nuclear receptor and downstream target genes (FGF21) following cardiac surgery can provide cardioprotection by increasing myocardial fatty acid oxidation and inhibiting NF-κB regulated pro-inflammatory responses. (duke.edu)
  • Heusch G: Myocardial ischaemia-reperfusion injury and cardioprotection in perspective. (spandidos-publications.com)
  • One such area of interest is the ability to modulate myocardial glucose uptake and its impact on cardioprotection. (biomedcentral.com)
  • 2017). The inhibition of hypothalamic inflammation by intracerebroventricular (ICV) administration of IKK2 inhibitor (IMD-0354) rectified PM2.5-induced glucose intolerance, IR, energy metabolism dysfunction, and attenuated peripheral inflammation in response to PM2.5 exposure (Song et al. (deepdyve.com)
  • 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)
  • MC-3 receptor and the inflammatory mechanisms activated in acute myocardial infarct. (ox.ac.uk)
  • We studied infarct size (IS) in rat hearts subjected to global ischemia-reperfusion (I/R) in vitro and endothelial function in healthy volunteers subjected to I/R of the upper arm. (ox.ac.uk)
  • 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)
  • 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)
  • Mechanistically this is accompanied by preservation of myocardial PPARα activity in AGS, which is significantly downregulated in the rat, and a metabolic phenotype consistent with the development of mitochondrial substrate flux "bottlenecks" in rats (myocardial accumulation of acylcarnitines and ceramides, organic acid profiles consistent with compromised citric acid cycle flux) compared to AGS. (duke.edu)
  • 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)
  • 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)
  • 22 have revealed that ASD attenuates neuroinflammatory responses in amyloid β-induced rats. (balkanmedicaljournal.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)
  • These data may open new avenues for therapeutic intervention against heart and possibly other organ ischemia-reperfusion injury. (ox.ac.uk)
  • This paper provides a review on the current evidence supporting the use of GLP-1 in experimental animal models and human trials with the ischemic and non-ischemic heart and discusses their molecular mechanisms and potential as a new therapeutic approach. (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)
  • A therapeutic drug that targets ischemia reperfusion (I/R) injury is needed and has yet to be developed. (biomedcentral.com)
  • 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)
  • 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)
  • There is substantial evidence that endothelial injury during organ procurement and preservation, caused by ischemia and subsequent reperfusion, results in endothelial dysfunction. (frontierspartnerships.org)
  • 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)
  • 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)
  • 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)
  • 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)
  • Donor pre-treatment with S-NO-HSA lead to reduced fibrosis and preservation of myocardial miR-126-3p and GATA2 levels in murine cardiac isografts 60 days after transplantation. (frontierspartnerships.org)
  • 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)
  • Investigation of the mechanisms activated by endogenous inhibitory pathways can lead to identification of novel targets for cardiovascular inflammatory pathologies. (ox.ac.uk)
  • 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)
  • There are still many unknown aspects of MIRI's key molecular mechanisms that merit further study through both in vivo and in vitro MIRI models to discover novel functional molecular targets and identify associated cardioprotective mechanisms, which is important for improving the current treatment of AMI and MIRI. (hindawi.com)
  • 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)
  • 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)
  • 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)
  • This study aimed to determine the potential myocardial protective effect and possible mechanism of action of D. odorifera essential oil (DOEO). (wjtcm.net)
  • This study was undertaken to investigate whether Res can protect the heart suffering from hypertrophy injuries induced by isoproterenol (ISO), and whether the protective effect is mediated by endoplasmic reticulum (ER) stress. (karger.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)
  • Our laboratory combines comparative biology approaches in multiple organisms with translational functional genomics to study the mechanisms underlying perioperative myocardial injury, with a particular emphasis on endogenous cardioprotective responses involving attenuation of nuclear factor-kappa B regulated inflammatory signaling and changes in myocardial fuel utilization. (duke.edu)
  • 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)
  • Abouzaki NA, Christopher S, Trankle C, Van Tassell BW, Carbone S, Mauro AG, Buckley L, Toldo S and Abbate A: Inhibiting the inflammatory injury after myocardial ischemia reperfusion with plasma-derived Alpha-1 Antitrypsin: A post hoc analysis of the VCU-α1RT study. (spandidos-publications.com)
  • Xia S, Sun Q, Zou Z, Liu Y, Fang X, Sun B, Wei S, Wang D, Zhang A, Liu Q. Ginkgo biloba extract attenuates the disruption of pro-and anti-inflammatory T-cell balance in peripheral blood of arsenicosis patients. (ijbs.com)
  • The present investigation describes a previously unknown mechanism showing that an imbalance of pro- and anti-inflammatory T cells is involved in the pathogenesis of arsenicosis and that a GBE exerts effects on arsenicosis through regulation of the pro- and anti-inflammatory T cell balance. (ijbs.com)
  • The key mechanisms underlying myocardial I/R injury include increased intracellular calcium concentration, sudden generation of reactive oxygen species (ROS) and inflammatory cytokines, adenosine triphosphate (ATP) depletion, and development of metabolic acidosis. (researchsquare.com)
  • Preliminary studies support a primary role for MyD88-signaling in mediating antimicrobial responses, potentially through augmentation of leukocyte metabolism, but the cellular and molecular mechanisms involved are unclear. (vumc.org)
  • Numerous apoptotic cardiomyocytes were found in ischemic fields in ischemia-reperfusion groups and werent observed in the sham-operated group. (ac.ir)
  • Cardiomyocytes were isolated and subjected to 6 h hypoxia followed by 18 h reperfusion. (biomedcentral.com)
  • Diabetes causes suppressed glucose oxidation leading to inefficient energy production, enhanced fatty acid metabolism, and increased susceptibility to myocardial ischemia and reperfusion injury. (biomedcentral.com)
  • The uncoupling of glycolysis and glucose oxidation induces lactate accumulation during myocardial ischemia/reperfusion (I/R) injury. (biomedcentral.com)
  • AKT inhibits fatty acid oxidation through down regulation of PPARα/PCG-1-dependent transcription [ 18 ] and promote glucose oxidation via Randle cycle mechanism [ 20 ]. (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)
  • 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)
  • The cardioprotective effects of DOEO were examined by histopathological observation, myocardial enzyme detection, peroxidation, anti-oxidant level detection, and related protein expression. (wjtcm.net)
  • These results suggest that IMD(1-53), like adrenomedullin, has cardioprotective effects against myocardial I/R injury. (phoenixpeptide.com)
  • Moreover, it was observed that, PGRN protects the heart against ischemia-reperfusion injury. (biomedcentral.com)
  • Interestingly, this winter cardioprotective phenotype is associated not only with suppression of metabolic demand, but also with a fuel shift from myocardial carbohydrate to fatty acid (FA) metabolism. (duke.edu)
  • We feel that developing strategies to help 'switch' myocardial metabolism to resemble that naturally occurring in mammalian hibernators represents a transformative approach that could ultimately have an important positive impact in patients undergoing cardiac surgery and transplantation, as well as in victims of cardiac arrest, stroke, trauma and hypothermia, in addition to fundamentally advancing the field of nuclear receptor biology and myocardial substrate metabolism under extremes of physiology. (duke.edu)
  • Glucose metabolism is an essential factor for myocardial self-repair after CPR. (dirjournal.org)
  • Impaired energy metabolism was closely related to myocardial damage after cardiopulmonary resuscitation (CPR). (dirjournal.org)
  • 18 F)-fluoro-D-glucose positron emission tomography/computed tomography can be used to evaluate myocardial damage after CPR by monitoring abnormal glucose metabolism. (dirjournal.org)
  • Glucose and fatty acids are important energy substrates for myocardial metabolism. (dirjournal.org)
  • 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)
  • 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)
  • Reperfusion with IMD significantly attenuated the I/R injury. (phoenixpeptide.com)
  • Compared to the myocardial ischemia group, the DOEO pretreatment groups had lower levels of myocardial injury, creatinine kinase, lactate dehydrogenase, alanine transaminase, aspartate transaminase, hydrogen peroxide, and nitric oxide, and higher levels of glutathione and superoxide dismutase. (wjtcm.net)
  • In addition, reperfusion with IMD(1-53)markedly attenuated the leakage of lactate dehydrogenase and malondialdehyde content in myocardia compared with I/R alone. (phoenixpeptide.com)
  • In addition, a significant decrease in the activities of myocardial injury markers i.e., creatine phosphokinase-MB (CK-MB isoenzyme) and lactate dehydrogenase (LDH) was also observed in the heart of ISP control group as compared to sham control. (scialert.net)
  • AMPK and AKT are synergistically activated by PLCA, which lead facilities glucose utilization, thereby attenuating lactate accumulation and cell death. (biomedcentral.com)
  • Hibernators such as arctic ground squirrels (AGS) depress their metabolic, heart, and respiratory rates as well as their core body temperature to enter a state called torpor during which they exhibit remarkable resistance to myocardial I/R injury and ventricular dysrhythmias normally associated with hypothermia. (duke.edu)
  • 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 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)
  • In addition, it has been shown that atorvastatin can protect the isolated mouse heart against reperfusion-induced injury [ 6 ]. (ac.ir)
  • 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)
  • The cAMP analogue 8-Br-cAMP-AM (8-Br) confers marked protection against global ischaemia/reperfusion of isolated perfused heart. (mdpi.com)
  • Cold ischemia and subsequent reperfusion injury are non-immunologic cornerstones in the development of graft injury after heart transplantation. (frontierspartnerships.org)
  • 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)
  • 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)
  • 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)
  • 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)
  • Because of overlapping mechanisms, this protection may be altered by glyceryl trinitrate (GTN), which is commonly used in the treatment of patients with chronic ischemic heart disease. (ox.ac.uk)
  • Coronary heart disease is a leading cause of death in the world and therapy to reduce injury is still needed. (biomedcentral.com)
  • With ischemia in coronary heart disease, impairment of the oxygen supply and metabolic disorder both occur [ 2 ]. (biomedcentral.com)
  • Cryonics patients frequently experience ischemic & reperfusion injury between the time when the heart stops and cryostorage begins. (benbest.com)
  • 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)
  • We observed that intracerebroventricular administration of IMD-0354 attenuated insulin resistance, inhibited macrophage polarization to M1 phenotype in epididymal adipose tissue in response to PM2.5 exposure. (deepdyve.com)
  • It has been shown that the Fas pathway is functional in cardiac myocytes and plays a critical role in myocardial death due to ischemia-reperfusion in vivo [ 4 ]. (ac.ir)
  • 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)
  • In addition, perfusion with IMD markedly attenuated the leakage of LDH, total protein and myoglobin from myocardia compared with I/R alone. (phoenixpeptide.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)
  • In this review, the clinical trials about curcumin supplementation on diabetes and DCM are presented, and the specific mechanisms by which curcumin might mitigate diabetes and DCM are fully discussed. (frontiersin.org)
  • 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)
  • However, combined application of RIC and long-term GTN treatment abolishes the individual protective effects of RIC and GTN treatment on ischemia-reperfusion injury, suggesting an interaction of clinical importance. (ox.ac.uk)
  • Venous thrombosis (sometimes called DVT, deep vein thrombosis) leads to a blood clot in the affected part of the body, while arterial thrombosis (and, rarely, severe venous thrombosis) affects the blood supply and leads to damage of the tissue supplied by that artery (ischemia and necrosis). (wikipedia.org)
  • Reperfusion injury refers to the tissue damage inflicted when blood flow is restored after an ischemic period of more than about ten minutes. (benbest.com)
  • but reperfusion may introduce additional harm to the tissue through a process known as ischemia/reperfusion injury. (cdc.gov)
  • 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)
  • For instance, some studies have suggested that in addition to antioxidant enzymes, nitric oxide synthases (NOSs), and other traditional enzymes, novel molecular targets such as mitochondria-targeting hydrogen sulfide (H 2 S) donor AP39 and its auxiliary targets have recently been identified as critical participants in H 2 S synthesis for modulating the postischemic cardiomyocyte survival in a manner independent of classical cytosolic signaling mechanisms [ 7 , 8 ]. (hindawi.com)
  • In this study, we demonstrate that MnSOD is down-regulated upon hydrogen peroxide treatment or ischemia/reperfusion (I/R) injury. (molcells.org)
  • The molecular events by which this precisely controlled increased reliance on myocardial FA utilization is cardioprotective in hibernators while it adversely impacts post-I/R cardiac efficiency and function in non-hibernators represent a significant knowledge gap. (duke.edu)
  • 13 ASD functions on different disease models, including neuropsychopathology, 14 Alzheimer's disease, 15 metabolic syndrome, 16 optic nerve injury, 17 atherosclerosis, 18 hepatic steatosis, 19,20 and leukemia. (balkanmedicaljournal.org)
  • Within two minutes of ischemia, extracellular pH can drop from about 7.3 to about 6.7. (benbest.com)
  • Finally, the activity of the sodium-potassium (Na+/K+) adenosine triphosphatase (ATPase) increases with maturation, which affects the sodium-calcium exchange mechanism. (medscape.com)
  • Ischemia is the condition suffered by tissues & organs when deprived of blood flow -- mostly the effects of inadequate nutrient & oxygen. (benbest.com)