• 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)
  • 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)
  • The findings of the present study indicated that inhibition of miR‑132 may ameliorate myocardial I/R injury by inhibiting oxidative stress and pyroptosis through activation of PGC‑1α/Nrf2 signalling by targeting SIRT1. (spandidos-publications.com)
  • Rationale: Both cardiomyocyte-restricted proteasome functional enhancement and pharmacological proteasome inhibition (PSMI) were shown to attenuate myocardial ischemia/reperfusion (I/R) injury. (elsevierpure.com)
  • Myocardial I/R injury may induce cell apoptosis and autophagy by activating oxidative stress and upregulating inflammatory mediators, ultimately resulting in irreversible fibrotic damage ( 3 ). (spandidos-publications.com)
  • 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)
  • 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)
  • Reports showed that mangiferin administration ameliorated isoproterenol-induced apoptosis [ 12 ] and hydrogen peroxide-induced cell injury [ 10 ] in cardiomyocytes. (kjpp.net)
  • Compared to rats, AGS display robust myocardial ischemic tolerance following DHCA (both reduced myocardial necrosis and apoptosis). (duke.edu)
  • 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)
  • 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)
  • 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 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)
  • 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)
  • Sun W, Wang Z, Sun M, Huang W and Wang Y and Wang Y: Aloin antagonizes stimulated ischemia/reperfusion-induced damage and inflammatory response in cardiomyocytes by activating the Nrf2/HO-1 defense pathway. (spandidos-publications.com)
  • It has been reported that SIRT1/peroxisome proliferator-activated receptor gamma coactivator (PGC)-1α/nuclear factor erythroid-2-related factor 2 (Nrf2) signalling can mediate oxidative stress, which plays an important role in myocardial I/R injury ( 14 , 15 ). (spandidos-publications.com)
  • Overall, the study showed that DOEO displayed myocardial protection by upregulating the NF-E2-related nuclear factor- antioxidant response element (Nrf2-ARE) and caspase pathways. (wjtcm.net)
  • Renal ischemia-reperfusion injury (IRI) is considered as a major cause of acute kidney injury. (frontiersin.org)
  • Renal ischemia-reperfusion injury (IRI) is a common pathophysiological phenomenon in clinical settings. (frontiersin.org)
  • 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)
  • 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)
  • There is substantial evidence that endothelial injury during organ procurement and preservation, caused by ischemia and subsequent reperfusion, results in endothelial dysfunction. (frontierspartnerships.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)
  • 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)
  • 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)
  • 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)
  • Moreover, it was observed that, PGRN protects the heart against ischemia-reperfusion injury. (biomedcentral.com)
  • Heusch G: Myocardial ischaemia-reperfusion injury and cardioprotection in perspective. (spandidos-publications.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)
  • An intravital model for imaging the adult and aged IR-injured beating heart in real time in vivo was used to demonstrate heightened basal and injury-induced neutrophil recruitment, and poorer blood flow, in the aged coronary microcirculation when compared with adult hearts. (jci.org)
  • Selectively stimulating ß1-adrenergic receptor attenuates rat myocardial ischemia/reperfusion injury in vivo by inhibiting high mobility group box 1 protein release]. (bvsalud.org)
  • Murine models of Matrigel plug and hindlimb ischemia were employed as in vivo angiogenic assays. (biomedcentral.com)
  • Interestingly, these exosomal effects were attenuated by using a colony stimulating factor 1 receptor (CSF-1R) inhibitor, BLZ945, in vitro and in vivo. (biomedcentral.com)
  • 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)
  • 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)
  • 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)
  • Several studies have been conducted on rodents to gain morphological, functional and molecular insights into sex-related differences in response to myocardial ischemic insults. (biomedcentral.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)
  • Ischemia was induced in male (M-Isch) and female (F-Isch) rats with sc. (biomedcentral.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)
  • 6]Huang X, Qiao F, Xue P. The protective role of microRNA-140-5p in synovial injury of rats with knee osteoar-thritis via inactivating the TLR4/Myd88/NF-κB signaling pathway[J]. Cell Cycle, 2019, 18:2344-2358. (magtechjournal.com)
  • This may be mechanistically explained by attenuated endothelial oxidative damage and VCAM-1 expression in IL-36Ra-treated mice. (jci.org)
  • The myocardial I/R model was established using C57BL/J6 mice. (spandidos-publications.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)
  • 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)
  • 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)
  • 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)
  • Numerous apoptotic cardiomyocytes were found in ischemic fields in ischemia-reperfusion groups and werent observed in the sham-operated group. (ac.ir)
  • 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)
  • Research done in animals shows that treatment with NAD+ precursors like NMN have cardioprotective effects against ischemia/reperfusion injury (4). (prohealth.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)
  • 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)
  • 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)
  • It was shown that functional Fas system contributes to apoptotic myocardial cell death in response to ischemia/reperfusion injury [ 4 , 5 ]. (ac.ir)
  • 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)
  • miR‑132 was significantly upregulated and SIRT1 was markedly downregulated in I/R myocardial tissues. (spandidos-publications.com)
  • Fas expression was significantly higher in the ischemia-reperfusion group as compared to sham-operated group, but was decreased significantly in atorvastatin treated group as compared with I/R group. (ac.ir)
  • 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)
  • 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)
  • 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)
  • Ischaemia-reperfusion (I/R) injury is the most important and common cause of myocardial damage and subsequent heart failure worldwide ( 1 , 2 ). (spandidos-publications.com)
  • Cold ischemia and subsequent reperfusion injury are non-immunologic cornerstones in the development of graft injury after heart transplantation. (frontierspartnerships.org)
  • Most myocardial infarctions, commonly known as heart attacks, happen in people once they get older, and aging makes it more difficult to recover from this type of injury. (prohealth.com)
  • 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)
  • This study aimed to determine the potential myocardial protective effect and possible mechanism of action of D. odorifera essential oil (DOEO). (wjtcm.net)
  • We assessed whether donor preservation with S-NO-HSA affects isograft injury and myocardial expression of GATA2 as well as miR-126-3p, which are considered protective against vascular and endothelial injury. (frontierspartnerships.org)
  • We first demonstrated the presence of IL-36(α/β) and its receptor (IL-36R) in ischemia/reperfusion-injured (IR-injured) mouse hearts and, interestingly, noted that expression of both increased with aging. (jci.org)
  • 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)
  • The volatile anesthetic desflurane (DES) effectively reduces cardiac infarct size following experimental ischemia/reperfusion injury in the mouse heart. (uni-wuerzburg.de)
  • 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)
  • 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)
  • Our study has highlighted sex-specific alterations in systolic and diastolic function shortly after ischemia, and provided a comprehensive look at the underlying proteomic changes and the influence of estrogens and their metabolites. (biomedcentral.com)
  • 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)
  • 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)
  • 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)
  • Interleukin-36 (IL-36), a newly discovered proinflammatory member of the IL-1 superfamily, may mediate this injury, but its role in the injured heart is currently not known. (jci.org)
  • 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)
  • Using intravital microscopy in a beating heart environment, we are able to directly observe thromboinflammatory events within myocardial microvessels, particularly the trafficking, adhesion kinetics (rolling / adhesion / transmigration) and cross-talk between leukocytes and platelets with each other and vascular endothelium. (birmingham.ac.uk)
  • 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)
  • 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)
  • The invention pertains to a polypeptide for the protection against heart ischemia-reperfusion injury. (justia.com)
  • One object of the present invention is to provide a therapy of heart ischemia-reperfusion injury by applying GLP-1 analogues which can be administered as single component and avoiding administration of the drug with a second compound. (justia.com)
  • The present invention is based on the surprising finding that the peptides of the invention have protective cardiovascular effects without simultaneous administration of other compounds, specifically they have protective effects on the heart against ischemia-reperfusion injury. (justia.com)
  • Postconditioning using N-Ac-GLP-1(7-34)amide N-terminally blocked and C-terminally truncated results in a limitation of ischemia-reperfusion injury in an isolated rat heart. (justia.com)
  • 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)
  • 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)
  • Furthermore, M2 polarization and angiogenesis were induced upon the administration of exosomes in mouse Matrigel plug and hindlimb ischemia (HLI) models. (biomedcentral.com)
  • This manuscript discusses some important biomarkers, such as neutrophil gelatinase-associated lipocalin (NGAL), kidney injury molecule 1 (KIM-1), liver-type FABP (L-FABP), proenkephalin (Penkid), metalloproteinase 2 (TIMP-2), insulin-like growth factor binding protein 7 (IGFBP7) and Dickkopf-3 (DDK3). (biolifesas.org)
  • 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)
  • Haematoxylin and eosin staining was performed to observe the injury of myocardial tissues. (spandidos-publications.com)
  • The microvascular and parenchymal organ damage induced upon ischemia tissue reperfusion is mainly attributed to the reactive oxygen-free radicals, and it has been demonstrated in many organs. (frontiersin.org)
  • FFPE tissue slides were scanned and analyzed digitally, while myocardial proteins were quantified by liquid chromatography-tandem mass spectrometry (LC-MS/MS) using isobaric labeling. (biomedcentral.com)
  • but reperfusion may introduce additional harm to the tissue through a process known as ischemia/reperfusion injury. (cdc.gov)
  • 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)
  • 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)
  • Results from clinical trials of dexmedetomidine on acute kidney injury (AKI) following adult cardiac surgery are controversial. (medscape.com)
  • The GRh2 pre‑treatment reduced the I/R‑ or H/R‑induced release of myocardial enzymes and the production of IL‑1β, IL‑18 and TNF‑α. (spandidos-publications.com)
  • Commercial kits were used to measure the levels of serum myocardial enzymes and inflammatory factors. (spandidos-publications.com)
  • Apparent histologic injury and elevated levels of serum myocardial enzymes and inflammatory factors were observed in the myocardial I/R model. (spandidos-publications.com)
  • Acute kidney injury (AKI) can result from a variety of etiologies (e.g., ischemia, toxicity, and sepsis) and is characterized by high rates of morbidity and mortality. (biolifesas.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)
  • Therefore, our research focuses on investigating the role of IL-36, age, and diabetes in myocardial IRI using intravital microscopy and laser speckle contrast imaging. (birmingham.ac.uk)