• In 1994, Gottlieb described the occurrence of programmed cell death (apoptosis) in the ischemic and reperfused heart, and highlighted that programmed cell death taking place during reperfusion is a regulated process that might be blocked to salvage myocardium. (wikipedia.org)
  • 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 vitro study showed that exendin-4 (the active ingredient of exenatide) attenuated HUVECs injury induced by high glucose, with improving cell viability and attenuating cell apoptosis. (hindawi.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)
  • It was previously demonstrated that targeting of a Na + -Ca 2+ exchanger by miR-132 was able to prevent apoptosis of cardiomyocytes under hypoxic conditions ( 11 ). (spandidos-publications.com)
  • At the end of reperfusion, Immunohistochemical detection of apoptotic cells was performed by using an in situ apoptosis detection kit. (vin.com)
  • Terminal deoxynucleotidyl transferase mediated dUTP nick end labeling assay was performed to detect cardiomyocyte apoptosis. (ijpsonline.com)
  • Dexmedetomidine pretreatment can obviously relieve myocardial ischemia-reperfusion injury and cardiomyocyte apoptosis in rats probably by activating the Janus kinase 2/signal transducers and activators of transcription 3 signaling pathway. (ijpsonline.com)
  • Therefore, we designed this study to see the influence of atorvastatin on cardiomyocyte apoptosis and Fas expression following acute I/R in vivo. (ac.ir)
  • Apoptosis of the cardiomyocytes was observed under electron microscopy and determined by optic microscopy with TUNEL (terminal deoxynucleotidyl transferase (TdT)-mediated dUTP nick end-labeling) staining. (ac.ir)
  • 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)
  • What is the pathophysiologic significance of cardiomyocyte apoptosis in heart failure? (latestfashiontips.com)
  • oxidative stress that occurs during reperfusion injury has been shown to induce apoptosis, over and above that induced by ischemia. (latestfashiontips.com)
  • ESTRÉS OXIDATIVO) desacoplando la membrana y dando lugar a APOPTOSIS y necrosis inducida por permeabilidad transmembrana mitocondrial, especialmente en los CARDIOMIOCITOS durante el DAÑO POR REPERFUSIÓN MIOCÁRDICA. (bvsalud.org)
  • In cardiomyocytes, the actions of NO are more complex as it can induce different, and sometimes opposing effects on cardiac functioning such as triggering apoptosis and improving left ventricular function. (medscape.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)
  • Meng X, Zhang L, Han B and Zhang Z: PHLDA3 inhibition protects against myocardial ischemia/reperfusion injury by alleviating oxidative stress and inflammatory response via the Akt/Nrf2 axis. (spandidos-publications.com)
  • The findings of the present study indicated that inhibition of miR‑132 may ameliorate myocardial I/R injury by inhibiting oxidative stress and pyroptosis through activation of PGC‑1α/Nrf2 signalling by targeting SIRT1. (spandidos-publications.com)
  • However, whether GRh2 has a protective effect on ischaemia/reperfusion (I/R) in the myocardium has yet to be elucidated. (spandidos-publications.com)
  • Ischemia-reperfusion injury (IRI) is a syndrome affecting the myocardium upon blood flow restoration following a sufficiently long interruption, such as encountered in a coronary thrombosis or heart surgery [1,2]. (justia.com)
  • 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)
  • The Canadian Cardiovascular Society (CCS) has developed a four-stage classification of acute atherothrombotic myocardial infarction (MI) based on the severity of the injury to the myocardium. (medscape.com)
  • Heusch G: Myocardial ischaemia-reperfusion injury and cardioprotection in perspective. (spandidos-publications.com)
  • The present study aimed to investigate the roles of miR‑132 in myocardial ischaemia/reperfusion (I/R) injury and the underlying mechanisms. (spandidos-publications.com)
  • 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)
  • Considering these results, we conclude that L-carnitine has a protective effect against cardiac ischemic reperfusion injuries as a reduction of apoptotic cardiomyocytes. (vin.com)
  • Numerous apoptotic cardiomyocytes were found in ischemic fields in ischemia-reperfusion groups and werent observed in the sham-operated group. (ac.ir)
  • Similarly, cardiomyocyte-specific Txnip deletion reduced infarct size after reversible coronary ligation. (jci.org)
  • 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)
  • We reported that there is infarct expansion after reperfusion, so once you open up the vessel, the heart attack actually gets larger. (medscape.com)
  • Increased infarct size after ischemia/reperfusion injury in Aspn-/- mice confirmed Aspn's contribution to cardiomyocyte viability. (beaumont.org)
  • Her subsequent work has explored the role of proteases and mitochondrial dysfunction in ischemia/reperfusion injury, and most recently, the importance of autophagy in mitigating reperfusion injury. (wikipedia.org)
  • Whereas mitochondrial ATP synthesis was minimally decreased by Txnip deletion, cellular ATP content and lactate formation were higher in Txnip-KO hearts after ischemia-reperfusion injury. (jci.org)
  • However, harmful stimuli (such as ischemia-reperfusion, oxidative stress, and toxic chemicals) can change the direction and efficiency of intercellular mitochondrial transfer. (frontiersin.org)
  • In addition, Aspn protected cardiomyocytes from hypoxia/reoxygenation-induced cell death and regulated mitochondrial bioenergetics in cardiomyocytes. (beaumont.org)
  • Cardiomyocytes were isolated and subjected to 6 h hypoxia followed by 18 h reperfusion. (biomedcentral.com)
  • Given the central role that mitochondria play during hypoxia, we hypothesized that Txnip deletion would enhance ischemia-reperfusion damage. (jci.org)
  • In vitro, HL-1 cells (mouse cardiomyocytes) received chamber hypoxia-oxygenation reperfusion (H/R) for 24H4R with/without DLC1β plasmid, before collection for protein/mRNA analyses. (uwo.ca)
  • 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)
  • Methods and Results-In vitro, neonatal rat cardiomyocytes were subjected to hypoxia-reoxygenation in the absence or presence of eEPCs with or without Tβ4 short hairpin RNA (shRNA) transfection. (elsevierpure.com)
  • Vascular endothelial cell (EC)-derived factors play an important role in endothelial-cardiomyocyte crosstalk and could save cardiomyocytes (CMs) from injury. (mdpi.com)
  • This review provides a current summary of the principal molecules, pathways, and mechanisms underlying cardiomyocyte and cardiac fibroblast crosstalk during ischemia/reperfusion injury. (unab.cl)
  • 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)
  • Ferroptosis plays an important regulatory role in the occurrence and development of many diseases, such as tumors, neurological diseases, acute kidney injury, ischemia/reperfusion, etc. (nature.com)
  • Apoptotic cardiomyocyte death is an increasingly recognized feature of congestive heart failure and acute myocardial infarction. (latestfashiontips.com)
  • Here, we initially confirmed our big dataset analysis through cells, mice, and clinical atrial biopsy samples to demonstrate increased Aspn expression after pressure overload or cardiac ischemia/reperfusion injury. (beaumont.org)
  • There are not enough reports about its anti-apoptotic effects during ischemia/reperfusion. (vin.com)
  • To evaluate the effects of dexmedetomidine on myocardial ischemia-reperfusion injury in rats and its anti-apoptotic role, as well as the mechanism by which it regulates Janus kinase 2/signal transducers and activators of transcription 3 signal. (ijpsonline.com)
  • We will investigate the effects of exenatide on vascular endothelial injury and nitrooxidative stress in hyperglycemia both in vivo and in vitro and explore the role of nitrooxidative stress in endothelium-protective action of exenatide. (hindawi.com)
  • Recent evidence has indicated that the vascular endothelial injury induced by hyperglycemia is associated with the enhanced nitrooxidative stress both in vivo and in vitro [ 3 - 6 ]. (hindawi.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)
  • The left anterior descending coronary artery was ligated to construct the model of myocardial ischemia-reperfusion. (ijpsonline.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)
  • The uncoupling of glycolysis and glucose oxidation induces lactate accumulation during myocardial ischemia/reperfusion (I/R) injury. (biomedcentral.com)
  • 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)
  • Nowadays, more and more studies have revealed that cells in the cardiovascular system (such as cardiomyocytes, vascular smooth muscle cells, endothelial cells, et al. (frontiersin.org)
  • In conclusion, this study demonstrates that exenatide treatment can alleviate the vascular endothelial injury, as well as attenuating the nitrooxidative stress in hyperglycemia, implying that the endothelium-protective effect of exenatide might be related to the reduction of nitrooxidative stress. (hindawi.com)
  • 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)
  • Her current projects are focused on the development of small-molecular cardioprotective agents for the treatment of reperfusion injury, mitochondria and stem cells in anthracycline-induced heart failure, rescue and role of complex I in myocardial ischemic injury, and microbial basis of cardiovascular disease. (wikipedia.org)
  • Atorvastatin has been shown to be cardioprotective in ischemia-reperfusion (I/R) injury. (ac.ir)
  • In the heart, cardiomyocytes, fibroblasts, and endothelial cells interact to form the cardiac tissue. (unab.cl)
  • Cardiac remodeling is also mediated by the factors secreted by cardiomyocytes and fibroblasts that are involved in the extensive reciprocal interactions between these cells. (unab.cl)
  • Activated fibroblasts during cardiac injury can alter the composition and activity of these ECM proteins. (beaumont.org)
  • 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)
  • 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 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)
  • Coronary heart disease is a leading cause of death in the world and therapy to reduce injury is still needed. (biomedcentral.com)
  • Conversely, Nrf1 overexpression protected the adult mouse heart from ischemia/reperfusion (I/ R ) injury. (nih.gov)
  • 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)
  • Cardiac ischemia-reperfusion injury (IRI) occurs intra-operatively during heart transplantation (HTx), underpinning graft survival. (uwo.ca)
  • The conducted study focuses on how we can reduce injury to the heart during heart transplantation. (uwo.ca)
  • Cardiac ischemia-reperfusion injury (IRI) occurs when transplanting a heart from donor to recipient. (uwo.ca)
  • By analyzing these questions, this research might be useful in humans to potentially reduce the rate of injury during heart transplantation. (uwo.ca)
  • 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)
  • 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)
  • In addition, it has been shown that atorvastatin can protect the isolated mouse heart against reperfusion-induced injury [ 6 ]. (ac.ir)
  • In recent years, extensive research has established that some immune cells either reside in the heart or have very complicated interactions with cardiomyocytes through permanent blood circulation. (biomedcentral.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)
  • 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)
  • Identifying the molecules and cellular signal pathways implicated in these processes will be crucial for creating effective tissue-preserving treatments during or after reperfusion. (unab.cl)
  • This is an important feature of apoptotic cell death/removal that occurs during development and cellular injury. (latestfashiontips.com)
  • In pathological conditions, damaged cells transfer dysfunctional mitochondria toward recipient cells to ask for help and take up exogenous functional mitochondria to alleviate injury. (frontiersin.org)
  • D. odorifera may be a potential candidate drug for treating myocardial ischemic injury. (wjtcm.net)
  • Gottlieb leads ongoing research focused on autophagy, mitophagy and biogenesis, with particular attention to the molecular basis of myocardial ischemia/reperfusion injury and in developing ways to mitigate damage. (wikipedia.org)
  • We tested the hypothesis that Aspn, being a TGFβ1 inhibitor, can attenuate fibrosis in mouse models of cardiac injury. (beaumont.org)
  • The nitric oxide donor S-nitroso-human-serum-albumin (S-NO-HSA) is known to attenuate myocardial ischemia-reperfusion (I/R)-injury. (frontierspartnerships.org)
  • The rate of aerobic oxidation of free fatty acids and glucose in cardiomyocytes is decreased, yet the rate of anaerobic glycolysis is enhanced. (dirjournal.org)
  • Her research primarily focuses on the molecular basis of myocardial ischemia/reperfusion injury and on developing ways to mitigate damage. (wikipedia.org)
  • 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)
  • However, despite numerous studies on myocardial I/R injury, deeper insight into the underlying mechanisms of myocardial I/R injury is needed. (spandidos-publications.com)
  • Numerous therapies to protect cardiac tissue from reperfusion-induced injury have been explored, and ample pre-clinical research has attempted to identify drugs or techniques to mitigate cardiac damage. (unab.cl)
  • moreover, in vivo grafts demonstrated reduced neutrophilic infiltrate/fibrosis/overall injury. (uwo.ca)
  • Nrf1 also protected human induced pluripotent stem cell-derived cardiomyocytes from doxorubicin-induced cardiotoxicity and other cardiotoxins. (nih.gov)
  • Results were confirmed via H9C2 (rat cardiomyocyte) cell lines. (uwo.ca)
  • One of the major contributors to myocardial cell injury is the increase in ROS as a result of ischemia/reperfusion (I/R) (Vanden Hoek et a/., 1996, 1997). (kzoo.edu)
  • It was shown that functional Fas system contributes to apoptotic myocardial cell death in response to ischemia/reperfusion injury [ 4 , 5 ]. (ac.ir)
  • The process is present during normal myocyte development and is activated in response to cell injury and results in the removal of the injured cell without damaging surrounding tissue. (latestfashiontips.com)
  • The degree of apoptotic cell death following ischemia/reperfusion may be reduced by the use of caspase inhibitors, antioxidants, and ischemic preconditioning. (latestfashiontips.com)
  • Recent studies have shown that ferroptosis is closely related to the pathophysiological processes of many diseases, such as tumors, nervous system diseases, ischemia-reperfusion injury, kidney injury, and blood diseases. (nature.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)
  • However, few studies have focused on the role of miR-132 in myocardial I/R injury and the underlying mechanisms. (spandidos-publications.com)