• 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)
  • 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)
  • Thus, inhibition of oxidative stress and myocardial apoptosis is beneficial in the treatment of myocardial I/R injury. (spandidos-publications.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, the aim of this study was to investigate apoptosis in various cardiac diseases: in hyperlipidemia induced atherosclerosis, in acute rejected heart transplants, in ischemia and reperfusion as well as in chronic hypoxia. (uni-frankfurt.de)
  • The morphologic changes seen in apoptosis include cell shrinkage, loss of cell-cell contacts, membrane blebbing, and nuclear condensation, terminating in the breakdown of the cell into apoptotic bodies that are phagocytosed by surrounding cells. (latestfashiontips.com)
  • Activation of the mitochondrial apoptotic process is regarded as the point of no return in apoptosis. (latestfashiontips.com)
  • oxidative stress that occurs during reperfusion injury has been shown to induce apoptosis, over and above that induced by ischemia. (latestfashiontips.com)
  • In conclusion, myocardial damage in MI is mainly due to ischemic necrosis and inflammatory mechanisms while apoptosis is the main mechanism of cell death in IR in addition to limited ischemic necrosis. (aku.edu)
  • As the indispensable role of apoptosis in MSC transplantation was raised, the benefits of MSC-derived apoptotic vesicles (apoVs) in several disease models have been proved. (biomedcentral.com)
  • In animal models, increased apoptosis accompanies both phases of ischemia and reperfusion [8]. (biomedres.us)
  • 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)
  • Ischaemia and reperfusion trigger cardiomyocyte death by necrosis and apoptosis. (mmu.ac.uk)
  • All of these factors are known to result in myocardial apoptosis(5) and the acceleration of allograft rejection or chronic allograft dysfunction. (researchsquare.com)
  • Pretreatment with baicalein dramatically reduced aspartate transaminase (AST) and alanine transaminase (ALT) serum levels, apoptosis in the liver, and elevated tumor necrosis factor-alpha (TNF-a), interleukin-1-beta (IL-1B), and interleukin-6 (IL-6) levels, which were caused by myocardial I/R. (remedies.news)
  • Reperfusion after cardiac ischemia increases cell death and infarct size (IS), called myocardial ischemia/reperfusion (I/R) injury, which is the main cause of myocardial injury during the cardiac surgery particularly in coronary artery bypass graft surgery ( 1 , 2 ). (spandidos-publications.com)
  • When subjected to myocardial ischemia-reperfusion injury, Caspase3 transgenic mice showed increased infarct size and a pronounced susceptibility to die. (uniroma5.it)
  • We also implicate Caspase3 in determining myocardial infarct size after ischemia-reperfusion injury, because its cardiomyocyte-specific overexpression increases infarct size. (uniroma5.it)
  • 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)
  • Short-term cardiac stress, induced by ischemia-reperfusion (I/R) injury resulted in impaired left ventricular (LV) recovery and increased infarct size in heterozygous Hmox1-deficient (Hmox1 +/− ) mice [ 55 ]. (springer.com)
  • H2S is a cardioprotective agent that has antioxidant, anti-inflammatory, and anti-apoptotic effects. (wikipedia.org)
  • Reperfusion triggers an inflammatory response and often results in oxidative damage. (wikipedia.org)
  • Standard histologic, immunohistochemical and Elisa techniques were used to study the histopathologic, oxidative, apoptotic and inflammatory changes in MI and IR. (aku.edu)
  • Important roles of inflammatory mediators in cardiac cell death by ischemia with or without reperfusion are well established [12-14]. (biomedres.us)
  • Recent evidence indicates that the PI3K/AKT signaling pathway may represent a compensatory mechanism in order to limit the pro-apoptotic and pro-inflammatory events in response to septic stimuli. (fapesp.br)
  • One of the primary causes of ARF is ischemia/reperfusion (I/R). Inflammatory process and oxidative stress are thought to be the major mechanisms causing I/R. MK-886 is a potent inhibitor of leukotrienes biosynthesis which may have anti-inflammatory and antioxidant effects through inhibition of polymorphonuclear leukocytes (PMNs) infiltration into renal tissues. (biomedcentral.com)
  • The end products of its enzymatic activity possess anti-oxidative, anti-apoptotic and anti-inflammatory properties. (springer.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)
  • The present study was designed to investigate the role of the miR‑133b‑5p in HPC‑induced cardioprotection and the underlying mechanisms involving caspase‑8 and caspase‑3 apoptotic signaling. (spandidos-publications.com)
  • Upregulation of miR‑133b‑5p contributes to HPC‑mediated cardioprotection in cardiomyocytes, and the mechanism may be associated with inhibition of caspase‑8 and caspase‑3 apoptotic signaling. (spandidos-publications.com)
  • Moreover, immunohistochemical experiments showed that DOEO remarkably increased the protein levels of NF-E2-related nuclear factor 2 (Nrf2) and heme oxygenase-1 (HO-1) and reduced the expression of apoptotic caspases, including caspase 3 and caspase 9. (wjtcm.net)
  • 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)
  • In this way, caspases recruit and activate proteins involved in the apoptotic process (eg, caspase-dependent endonuclease), inactivate survival proteins (eg, the extracellularly responsive kinases and the DNA repair enzyme poly-ADP-ribosyl polymerase), and act directly on cytoskeletal proteins, resulting in plasma membrane changes. (latestfashiontips.com)
  • The Bcl-2 proteins influence cell survival primarily by controlling the mitochondrial response to apoptotic signals, although direct inhibition of caspase activity may occur. (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)
  • Our IR model showed enhanced pro-apoptotic mediators like cleaved caspase-3 (P=0.005) and cytochrome c in the myocardium as compared to the MI model. (aku.edu)
  • Hypoxia/reoxygenation (H/R) as well as hypoxic preconditioning (HPC) is widely used for simulating in vivo myocardial I/R and ischemic preconditioning (IPC) in a cell culture model. (spandidos-publications.com)
  • 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)
  • Cardiomyocytes were isolated and subjected to 6 h hypoxia followed by 18 h reperfusion. (biomedcentral.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)
  • Adult rats were subjected to myocardial ischemia/reperfusion (I/R) injury with or without ischemic preconditioning (IPC), and the level of miR‑133b‑5p in myocardium was measured. (spandidos-publications.com)
  • Following myocardial I/R injury, the expression of miR‑133b‑5p was decreased in myocardium, while this decrease was restored by IPC. (spandidos-publications.com)
  • Restoration of blood supply, termed reperfusion, has been used to treat ischemic myocardium and prevent further tissue damage. (spandidos-publications.com)
  • Reperfusion has the potential to salvage ischemic myocardium but paradoxically can cause injury, a phenomenon called as 'reperfusion injury' (IR). (aku.edu)
  • Improved heart function was accompanied by reduced inflammation, including decreased cell-migration into the infarcted myocardium and improved cell survival in the infarct border zone as detected by reduced expression of pro-apoptotic proteins in the acute phase and reduced active caspase3 5 days after I/R. (isth.org)
  • 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)
  • Reperfusion and neurovascular dysfunction in stroke: from basic mechanisms to potential strategies for neuroprotection. (wanfangdata.com.cn)
  • Mitochondrial Dysfunction and Autophagy in Hepatic Ischemia/Reperfusion Injury. (wanfangdata.com.cn)
  • Mitochondrial dysfunction plays a central role in mediating both the necrotic and apoptotic components of reperfusion injury. (elsevierpure.com)
  • Glucose-insulin-potassium (GIK) has long been advocated as an adjunctive treatment for patients with cardiac dysfunction during episodes of ischemia and reperfusion. (biomedcentral.com)
  • discovered that constant infusion of MB counteracts early myocardial dysfunction and derangement of hemodynamics and gas exchange by inhibition of nitric oxide pathway within an ovine endotoxemia model [48]. (immune-source.com)
  • In heart transplantation, donor hearts inevitably suffer from ischemia/reperfusion (I/R) injury, which leads to primary graft dysfunction and affects patients' survival rate. (researchsquare.com)
  • Key apoptotic pathway intermediates and inflammation markers IL-6, IL-8, and tumor necrosis factor (TNF) were quantified by western blot analyses, while miR-126 expression was tracked by quantitative polymerase chain reaction (qPCR). (biomedres.us)
  • 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)
  • Rats were randomly divided into 3 groups: control group (n=3), myocardial ischemia without reperfusion (PI group, n=3), and myocardial ischemia with reperfusion (IR group, n=4). (elsevierpure.com)
  • For the study, the research team pretreated rats with 3, 10, or 30 milligrams per kilogram (mg/kg) baicalein 10 minutes before myocardial I/R. (remedies.news)
  • They induced myocardial I/R in rats via occlusion of the left anterior descending coronary artery for 40 minutes and reperfusion for three hours. (remedies.news)
  • Apoptotic cell death follows well-defined time-depend-ent processes, which result in changes in the plasma membrane, proteolysis of intracellular proteins, loss of mitochondrial function, and characteristic DNA cleavage. (latestfashiontips.com)
  • Cyclophilin D-dependent mitochondrial permeability transition regulates some necrotic but not apoptotic cell death. (wanfangdata.com.cn)
  • The mitochondrial permeability transition pore and its role in myocardial ischemia reperfusion injury [J].2015,78. (wanfangdata.com.cn)
  • However, harmful stimuli (such as ischemia-reperfusion, oxidative stress, and toxic chemicals) can change the direction and efficiency of intercellular mitochondrial transfer. (frontiersin.org)
  • As a result, shape measurement parameters for the quantitative analysis of mitochondrial swelling could be very effective for evaluating the myocardial injury. (elsevierpure.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)
  • However, while myocardial reperfusion is well established, the process itself can trigger myocardial reperfusion injury by causing further cardiomyocyte death through multiple pathophysiological mechanisms [ 3 - 5 ]. (hindawi.com)
  • Conceptual diagram of the development and unknown mechanisms of myocardial ischemia-reperfusion injury. (hindawi.com)
  • 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)
  • Aldehyde dehydrogenase 2 (ALDH2) rescues myocardial ischaemia/reperfusion injury: role of autophagy paradox and toxic aldehyde. (wanfangdata.com.cn)
  • Calpain 2-mediated autophagy defect increases susceptibility of fatty livers to ischemia-reperfusion injury. (wanfangdata.com.cn)
  • Induction of autophagy reduces ischemia/reperfusion injury in steatotic rat livers [J].2017,216. (wanfangdata.com.cn)
  • A team of researchers from the National Yang-Ming University School of Medicine in Taipei, Taiwan examined baicalein to see if it can reduce liver injury induced by myocardial ischemia and reperfusion (I/R). Their study was published in The American Journal of Chinese Medicine . (remedies.news)
  • Overall, the results suggested that baicalein can reduce liver injury induced by myocardial I/R. (remedies.news)
  • Glucose-insulin-potassium (GIK) has been advocated in the setting of acute coronary syndrome (ACS) to reduce ischemia-related arrhythmias and myocardial injury. (biomedcentral.com)
  • The left anterior descending coronary artery was ligated to construct the model of myocardial ischemia-reperfusion. (ijpsonline.com)
  • Cellular injury was evaluated by detecting cell viability, lactate dehydrogenase (LDH) activity and apoptotic rate. (spandidos-publications.com)
  • The uncoupling of glycolysis and glucose oxidation induces lactate accumulation during myocardial ischemia/reperfusion (I/R) injury. (biomedcentral.com)
  • The mitochondria has been known to protect the heart from ischemic-reperfusion injury through the opening of the ATP-sensitive K+ channel. (wikipedia.org)
  • In this study, we characterized the morphological changes in heart mitochondria caused by the duration and severity of ischemia utilizing particle shape analysis on atomic force microscopy (AFM) topographic images. (elsevierpure.com)
  • From the morphological and nano-mechanical changes in heart mitochondria, we suggested that the outer membranes of mitochondria were broken by myocardial ischemic injury before they became swollen, and the swelling might be correlated with the ischemic injury. (elsevierpure.com)
  • Da in der Zellkultur protektive Effekte von NO gezeigt werden konnten, wurde deren physiologische Relevanz in der durch Ischämie/Reperfusion induzierten Apoptose ex vivo im Langendorff-Rattenherzen untersucht. (uni-frankfurt.de)
  • MB research in ischemic heart stroke While low-dose MB has been shown to lessen neurobehavioral impairment in neurodegenerative illnesses (Parkinson's disease [23 29 Alzheimer disease [30-32]) the neuroprotective ramifications of MB on cerebral ischemia in vivo had been only. (immune-source.com)
  • Despite inducing ultrastructural damage, Caspase3 does not trigger a full apoptotic response in the cardiomyocyte. (uniroma5.it)
  • Heart failure is characterized by a significant increase in apoptotic myocyte death in spite of the enhanced expression of antiapoptotic gene products in the cells. (latestfashiontips.com)
  • Moreover, it was observed that, PGRN protects the heart against ischemia-reperfusion injury. (biomedcentral.com)
  • This anatomic condition is characterized by diastolic overloading, sarcomere stretching, apoptotic cell death, and side-to-side slippage of myocytes within the wall. (latestfashiontips.com)
  • However, the role of SA in myocardial I/R injury is unclear. (spandidos-publications.com)
  • However, the role of SA in myocardial I/R injury remains to be elucidated. (spandidos-publications.com)
  • While the bioactive glycerophospholipid lysophosphatidic acid (LPA) plays a well-known role in atherosclerotic disease, its role in myocardial function remains virtually unexplored. (lsuhs.edu)
  • In addition, IGF-I inhibits apoptotic cell death and therefore plays an important role as a cell survival factor. (mmu.ac.uk)
  • Nitric oxide generation during reperfusion and ischemia plays a substantial role in ischemic and reperfusion injury [56]. (immune-source.com)
  • 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)
  • The cardioprotective effects of DOEO were examined by histopathological observation, myocardial enzyme detection, peroxidation, anti-oxidant level detection, and related protein expression. (wjtcm.net)
  • BACKGROUND: C1q/tumor necrosis factor-related protein 5 (CTRP5) has been reported to be a crucial regulator in cardiac ischemia/reperfusion (I/R) injury. (bvsalud.org)
  • We have demonstrated that HNE adduction of AIFm2 shifts the function of AIFm2 from an NADH oxidoreductase to a pro-apoptotic protein. (lsuhs.edu)
  • This is an important feature of apoptotic cell death/removal that occurs during development and cellular injury. (latestfashiontips.com)
  • The results support significant roles for miR-126 in regulating cardiac myocyte survival pathways and cell death during exposure to simulated ischemia and acidosis. (biomedres.us)
  • There is proof that MB lowers or inhibits nitric oxide era might have the aftereffect of neuroprotection in ischemia/reperfusion damage. (immune-source.com)
  • This study aimed to determine the potential myocardial protective effect and possible mechanism of action of D. odorifera essential oil (DOEO). (wjtcm.net)