Mechanisms of myocardialOxidative stress and inflammatoryInfarctionCardioprotectionMyocardiumInhibitionAcuteNrf2HypoxiaEnzymesCoronaryApoptosisHeart failureProteinsProtectiveRoleModelGlobalTreating myocardial infarctionInflammatory responseAcuteAttenuateInflammationTissuesEndothelial cellsOxidativeCardiomyocytesRenalIschaemicMiceCardiacMortalitySignificantlyMolecularActivationFunctionLiver injuryGeneTherapyEffectInvolved in variousPatientsControlResultsHigh
Mechanisms of myocardial2
- Conceptual diagram of the development and unknown mechanisms of myocardial ischemia-reperfusion injury. (hindawi.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)
Oxidative stress and inflammatory1
- 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)
Infarction5
- Worldwide morbidity and mortality from acute myocardial infarction (AMI) and related heart failure remain high. (hindawi.com)
- Among clinical emergency events, ST-segment elevation (STE) or the non-STE electrocardiogram diagnosis of acute myocardial infarction (AMI) is particularly common worldwide, with a staggering number of annual first episodes as well as recurrent ones [ 1 ]. (hindawi.com)
- GRh2 reduced the area of myocardial infarction and the histological changes in the myocardium and improved cardiac functions. (spandidos-publications.com)
- Despite improvements in revascularization after a myocardial infarction, coronary disease remains a major contributor to global mortality. (ku.dk)
- Despite substantial declines in mortality following myocardial infarction (MI), subsequent left ventricular remodeling (LVRm) remains a significant long-term complication. (researchgate.net)
Cardioprotection2
- 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)
- Heusch G: Myocardial ischaemia-reperfusion injury and cardioprotection in perspective. (spandidos-publications.com)
Myocardium4
- 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)
- However, whether GRh2 has a protective effect on ischaemia/reperfusion (I/R) in the myocardium has yet to be elucidated. (spandidos-publications.com)
Inhibition1
- 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)
Acute2
- Oral dosing of rats with SCN-, before acute ischemia-reperfusion injury (30 min occlusion, 24 h or 4 week recovery), significantly reduced the infarct size as a percentage of the total reperfused area (54% versus 74%), and increased the salvageable area (46% versus 26%) as determined by MRI imaging. (ku.dk)
- These data indicate that elevated levels of the MPO substrate SCN-, which can be readily modulated by dietary means, can protect against acute ischemia-reperfusion injury. (ku.dk)
Nrf23
- 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 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)
Hypoxia2
- 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)
- 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)
Enzymes3
- 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)
Coronary1
- 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)
Apoptosis1
- 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)
Heart failure1
- 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)
Proteins1
- Supplementation also decreased antibody recognition of HOCl-damaged myocardial proteins. (ku.dk)
Protective1
- We tested the hypothesis that 8-Br is also protective under clinically relevant conditions (regional ischaemia) when applied either before ischemia or at the beginning of reperfusion, and this effect is associated with the mitochondrial permeability transition pore (MPTP). (mdpi.com)
Role1
- However, few studies have focused on the role of miR-132 in myocardial I/R injury and the underlying mechanisms. (spandidos-publications.com)
Model1
- The myocardial I/R model was established using C57BL/J6 mice. (spandidos-publications.com)
Global1
Treating myocardial infarction1
- Therefore, inhibition of cardiomyocyte apoptosis may improve cardiac function and alleviate MIRI which is of clinical significance for treating myocardial infarction. (hindawi.com)
Inflammatory response3
- It also induces myocardial apoptosis, inflammatory response, and oxidative stress resulting in severe arrhythmia, cardiac failure, and even sudden cardiac death [ 4 ]. (hindawi.com)
- Our results indicate that geniposide can reduce the area of myocardial infarction, improve heart function, and inhibit the inflammatory response in mice after MI/RI. (biomedcentral.com)
- Xiong J, Yuan YJ, Xue FS, Wang Q, Cheng Y, Li RP, Liao X and Liu JH: Postconditioning with α7nAChR agonist attenuates systemic inflammatory response to myocardial ischemia-reperfusion injury in rats. (spandidos-publications.com)
Acute2
- Acute ischemic injury in limbs may occur due to crush syndrome, compartment syndrome, and vascular diseases and injury as in acute peripheral arterial occlusion, caused by a diverse array of pathological conditions. (bvsalud.org)
- Furthermore, the effects of IR-injured skeletal muscle in clinical conditions such as compartment syndrome or crush syndrome may induce rhabdomyolysis and are associated with so-called remote injuries as acute kidney dysfunction. (bvsalud.org)
Attenuate1
- In conclusion, hypercholesterolemia could aggravate myocardial ischemia/reperfusion injury, attenuate cardioprotection of ischemic preconditioning and eliminate cardioprotection from α7nAChR agonist postconditioning by enhancing inflammation and inhibiting PI3K/Akt/eNOS pathway. (spandidos-publications.com)
Inflammation2
- Targeting Myeloperoxidase (MPO) Mediated Oxidative Stress and Inflammation for Reducing Brain Ischemia Injury: Potential Application of Natural Compounds. (thieme-connect.com)
- Ischemia/reperfusion injury in skeletal muscle leads to sterile inflammation and affects structure and function permanently. (bvsalud.org)
Tissues1
- In our study, geniposide can significantly inhibit NLRP3 inflammasome activation via the AMPK signaling pathway and inhibit pyroptosis of cardiomyocytes in myocardial tissues. (biomedcentral.com)
Endothelial cells4
- 1. Brg1 deficiency in vascular endothelial cells blocks neutrophil recruitment and ameliorates cardiac ischemia-reperfusion injury in mice. (nih.gov)
- 2. BRG1 regulates NOX gene transcription in endothelial cells and contributes to cardiac ischemia-reperfusion injury. (nih.gov)
- Endothelium was an active early participant in ischemia-reperfusion (IR) injury and endothelial cells were particularly susceptible to and actively participate in IR injury [ 8 - 10 ]. (hindawi.com)
- In the present study, we checked whether SCU could also protect endothelial cells against simulated IR injury, 12 h hypoxia followed by 12 h reoxygenation. (hindawi.com)
Oxidative2
- HE staining, 2,3,5-triphenyltetrazolium chloride (TTC) staining, echocardiography, oxidative stress and myocardial enzyme detection were used to evaluate the cardioprotective effect of geniposide. (biomedcentral.com)
- Protective Effects of Salidroside against Carbon Tetrachloride (CCl(4))-Induced Liver Injury by Initiating Mitochondria to Resist Oxidative Stress in Mice. (thieme-connect.com)
Cardiomyocytes1
- SCU was found to have protective effects on cardiomyocytes against ischemic injury [ 6 , 7 ]. (hindawi.com)
Renal3
- 3. BRG1 regulates endothelial-derived IL-33 to promote ischemia-reperfusion induced renal injury and fibrosis in mice. (nih.gov)
- 9. Endothelial-specific deletion of Brahma-related gene 1 (BRG1) assuages unilateral ureteral obstruction induced renal injury in mice. (nih.gov)
- Progression to renal damage by ischemia-reperfusion injury (IRI) is the result of the dysregulation of various tissue damage repair mechanisms. (researchgate.net)
Ischaemic3
- Schematic of proposed mechanism of myocardial ischaemic. (researchgate.net)
- Interventions such as ischaemic pre and postconditioning protect against myocardial ischaemia reperfusion injury. (researchgate.net)
- Hausenloy DJ and Yellon DM: Ischaemic conditioning and reperfusion injury. (spandidos-publications.com)
Mice2
- 16. Endothelial Cx40 limits myocardial ischaemia/reperfusion injury in mice. (nih.gov)
- Recently, targeted myocardial delivery of the GDF11 gene in aged mice was found to reduce h. (researchgate.net)
Cardiac3
- 12. Selectin-targeting glycosaminoglycan-peptide conjugate limits neutrophil-mediated cardiac reperfusion injury. (nih.gov)
- 18. Megakaryocytic Leukemia 1 Bridges Epigenetic Activation of NADPH Oxidase in Macrophages to Cardiac Ischemia-Reperfusion Injury. (nih.gov)
- Serum lactate dehydrogenase (LDH), creatine kinase isoenzyme MB (CK-MB), cardiac troponin I (cTnI), tumor necrosis factor α (TNF‑α) and interleukin‑6 (IL‑6) levels after ischemia/reperfusion were assayed. (spandidos-publications.com)
Mortality1
- Although patients with AMI may undergo timely reperfusion therapy, the mortality of MIRI is still 10% [ 5 ]. (hindawi.com)
Significantly3
- Compared with the NI group, serum LDH, CK‑MB, cTnI, TNF‑α and IL‑6 levels and infarct size were significantly decreased, and myocardial p‑Akt/Akt and eNOS/GAPDH ratios were significantly increased in the NIPC and NPNU groups. (spandidos-publications.com)
- however, myocardial p‑Akt/Akt and eNOS/GAPDH ratios did not significantly change in the HIPC group. (spandidos-publications.com)
- Results of MTT assay showed that pretreatment of SCU at doses of 1, 5, and 10 μ M for 2 h could significantly inhibit the decrease in cell viability of HCMECs induced by HR injury. (hindawi.com)
Molecular1
- However, the underlying molecular mechanisms of 6-G myocardial protection are not known. (hindawi.com)
Activation3
- NLRP3 inflammasome activation and pyroptosis play a significant role in myocardial ischemia reperfusion injury (MI/RI). (biomedcentral.com)
- 13. Inhibition of BRD4 Reduces Neutrophil Activation and Adhesion to the Vascular Endothelium Following Ischemia Reperfusion Injury. (nih.gov)
- These involve the activation of Jak/STAT3 and PI3K/Akt, which subsequently decreases mitochondrial permeability transition pore (mPTP) opening and increases mitochondrial K ATP (Mito K ATP ) channel opening, which attenuates myocardial ischaemia reperfusion injury. (researchgate.net)
Function1
- Myocardial ischemia/reperfusion injury (MIRI) causes damage to the function, metabolism, and structure of the heart. (hindawi.com)
Liver injury1
Gene1
- 4. Proinflammatory stimuli engage Brahma related gene 1 and Brahma in endothelial injury. (nih.gov)
Therapy2
- Percutaneous coronary intervention (PCI) and thrombolytic therapy can recover myocardial blood supply in timely manner. (hindawi.com)
- Rossello X, Lobo-Gonzalez M and Ibanez B: Editor's choice-pathophysiology and therapy of myocardial ischaemia/reperfusion syndrome. (spandidos-publications.com)
Effect1
- AMPK antagonist or agonist and siRNA downregulation of TXNIP or NLRP3 were also verify the effect of geniposide against H/R injury. (biomedcentral.com)
Involved in various1
- Myocardial ischemia/reperfusion injury (MI/RI) is involved in various pathological states. (biomedcentral.com)
Patients1
- Myocardial ischaemia reperfusion injury is the leading cause of death in patients with cardiovascular disease. (researchgate.net)
Control2
- Subcellular fractions of cells treated with vehicle control, 1 μ M SCU, HR injury, or 1 μ M SCU + HR injury were separated by ultracentrifugation. (hindawi.com)
- At the same time, proteins differentially expressed between control and HR group were also identified to provide information about possible proteins involved in HR injury. (hindawi.com)
Results2
- These results might be important for developing novel strategies for preventing myocardial I/R injury. (hindawi.com)
- Iatrogenic revascularization and restoration of perfusion results paradoxically in aggravated tissue injury. (bvsalud.org)
High1
- Despite of many years of efforts to reduce ischemia-reperfusion injury, MI/RI-associated death rate remains persistently high. (biomedcentral.com)