• It has previously been demonstrated that phosphatidylinositol‑3‑kinase (PI3K)/Akt and cleaved caspase‑3 serve critical roles in the apoptosis of cardiac myocytes following ischemia/reperfusion injury. (spandidos-publications.com)
  • Stephanou A, Brar B, Liao Z, et al: Distinct initiator caspases are required for the induction of apoptosis in cardiac myocytes during ischaemia versus reperfusion injury. (spandidos-publications.com)
  • Scarabelli TM, Stephanou A, Pasini E, et al: Different signaling pathways induce apoptosis in endothelial cells and cardiac myocytes during ischemia/reperfusion injury. (spandidos-publications.com)
  • Townsend PA, Scarabelli TM, Pasini E, et al: Epigallocatechin-3-gallate inhibits STAT-1 activation and protects cardiac myocytes from ischemia/reperfusion-induced apoptosis. (spandidos-publications.com)
  • 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)
  • Cardiac ischemia/reperfusion (I/R) injury is a serious disease and threatens human health [ 1 ]. (hindawi.com)
  • Despite the recent surge about miRNA discoveries for cardiac I/R injury, there is still very little known about the mechanism details because of the complexity of cellular events and the interference of other risk factors. (hindawi.com)
  • Endothelin-1 (ET-1) is believed to play an important role in cardiac ischaemia/reperfusion injury. (portlandpress.com)
  • Elevations in the expression of this enzyme may help to explain the role of the ET system in the pathogenesis of ischaemia/reperfusion injury following cardiac surgery and transplantation. (portlandpress.com)
  • Here, we review the information linking the adaptor protein p66Shc with cardiac injury induced by ischaemia and reperfusion (I/R), including the contribution of risk factors, such as metabolic syndrome and ageing. (nih.gov)
  • Epigallocatechin‑3‑gallate (EGCG), the predominant catechin component of green tea, has been reported to have potential cardioprotective effects in primary cultures of cardiac myocytes exposed to I/R injury, mediated through inhibition of signal transducers and activators of transcription‑1 activity. (spandidos-publications.com)
  • In the present study, the protective effects of EGCG with zinc were assessed on cultures of rat cardiac myoblasts exposed to hypoxia/reoxygenation (H/R) injury. (spandidos-publications.com)
  • Since EGCG + Zn2+ may, at least in part, protect cardiac myocytes against H/R‑induced apoptotic cell death, the PI3K/Akt pathway of EGCG may be enhanced by its interactions with zinc during H/R injury. (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)
  • Reperfusion treatment has a potential risk of worsening tissue damage after ischemia, which can accelerate the deterioration of cardiac function [ 2 ]. (hindawi.com)
  • 6-Gingerol (6-G) is known to alleviate myocardial ischemia/reperfusion injury. (hindawi.com)
  • Myocardial ischemia/reperfusion injury (MIRI) causes damage to the function, metabolism, and structure of the heart. (hindawi.com)
  • 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)
  • Wu Y, Liu H and Wang X: Cardioprotection of pharmacological postconditioning on myocardial ischemia/reperfusion injury. (spandidos-publications.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)
  • Rats were subjected to I/R in the presence or absence of 6-G and the changes of cardiac function, infarct size and histopathological changes, and the levels of cardiac troponin T, creatine kinase-MB, and myocardial apoptosis were examined. (hindawi.com)
  • We found that 6-G (6 mg/kg) pretreatment significantly improved heart function and ameliorated infarct size and histopathological changes and cardiac troponin T and creatine kinase-MB levels induced by I/R. Moreover, pretreatment with 6-G significantly inhibited myocardial apoptosis and caspase-3 activation induced by I/R. 6-G also upregulated expression of PI3K, p-Akt, and Akt in myocardial tissues. (hindawi.com)
  • These are the most effective treatments for saving the endangered myocardium, reducing the infarct size, maintaining cardiac function, and alleviating ventricular remodeling after infarction [ 3 ]. (hindawi.com)
  • After prolonged periods (up to 18 h) of cold ischaemic lung preservation without reperfusion, a high percentage of cell necrosis (but not apoptosis) can be observed 12 , 13 . (ersjournals.com)
  • Ischaemic postconditioning confers cardioprotection through the survivor activating factor enhancement (SAFE) and reperfusion injury salvage kinase (RISK) pathways. (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)
  • The purpose of this review is to summarise recent findings on complement activation and acquired brain or spinal cord injury, i.e. ischaemic-reperfusion injury or stroke, traumatic brain injury (TBI) and spinal cord injury (SCI), highlighting the potential for complement-targeted therapeutics to alleviate the devastating consequences of these neurological conditions. (biomedcentral.com)
  • Andreadou I, Iliodromitis EK, Lazou A, Görbe A, Giricz Z, Schulz R and Ferdinandy P: Effect of hypercholesterolaemia on myocardial function, ischaemia-reperfusion injury and cardioprotection by preconditioning, postconditioning and remote conditioning. (spandidos-publications.com)
  • Lung tissue necrosis after prolonged ischaemia is known to worsen lung function, which was believed to be due largely to adjacent tissue inflammation. (ersjournals.com)
  • Tissue necrosis after lung ischaemia-reperfusion injury has been recognised to be associated with significantly worsened lung function, related to the high degree of inflammation. (ersjournals.com)
  • Injury to the central nervous system (CNS) elicits a complex series of pathophysiological events, including ischaemia, excitotoxicity and inflammation. (biomedcentral.com)
  • The current review highlights the latest research findings in apoptosis after acute lung ischaemia-reperfusion injury. (ersjournals.com)
  • It also induces myocardial apoptosis, inflammatory response, and oxidative stress resulting in severe arrhythmia, cardiac failure, and even sudden cardiac death [ 4 ]. (hindawi.com)
  • The current literature on the mechanism and pathways involved in pulmonary dysfunction and, in particular, its relationship with apoptosis after lung ischaemia-reperfusion is briefly reviewed here. (ersjournals.com)
  • A better understanding of lung apoptosis, as well as the upstream pathways, may help in the development of therapeutic strategies that could benefit patients undergoing cardiac and lung transplantation. (ersjournals.com)
  • The final pathways, after lung ischaemia and reperfusion, leading to cellular damage, necrosis or apoptosis of the pulmonary epithelium remain to be fully elucidated. (ersjournals.com)
  • Since the late 1990s, scientists have recognised that the different processes following ischaemia-reperfusion, although closely related, cause lung injury by activation of different inflammatory pathways 2 , 4 , 6 . (ersjournals.com)
  • Growth differentiation factor 11 (GDF11) is a member of the transforming growth factor beta 1 (TGF-β1) superfamily that reverses age-related cardiac hypertrophy, improves muscle regeneration and angiogenesis, and maintains progenitor cells in injured tissue. (researchgate.net)
  • This study shows that, through antagonism of TP signaling, NTP42:KVA4 attenuates experimental PAH pathophysiology, not only alleviating pulmonary pathologies but also reducing RV remodeling, promoting beneficial hypertrophy, and improving cardiac function. (frontiersin.org)
  • More recently our work is addressing the problems caused by ischaemia reperfusion (I/R) injury in the heart. (ncl.ac.uk)
  • In addition, in collaborative studies, we are investigating whether fractalkine, a protein that is dynamically regulated in cardiac I/R injury in patients, can be used as a target for therapy. (ncl.ac.uk)
  • The central role of lung ischaemia-reperfusion injury in pulmonary dysfunction after cardiac surgery, particularly thoracic organ transplantation, has been well recognised. (ersjournals.com)
  • Post-operative pulmonary dysfunction following the use of cardiopulmonary bypass is a frequently observed phenomenon that is associated with lung ischaemia-reperfusion injury 2 , 3 . (ersjournals.com)
  • However, understanding of the complex pathophysiology of ischaemia-reperfusion-induced lung injury remains incomplete. (ersjournals.com)
  • Since the mid-1980s, the role of neutrophils, free radicals and other inflammatory mediators in ischaemia-reperfusion injury has been extensively investigated 4 . (ersjournals.com)
  • Nevertheless, these mediators appear to contribute only in part to lung ischaemia-reperfusion injury. (ersjournals.com)
  • 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)
  • Myocardial ischaemia reperfusion injury is the leading cause of death in patients with cardiovascular disease. (researchgate.net)
  • as a feasible method for reduction of myocardial ischaemia-reperfusion (IR) injury. (researchgate.net)
  • Ischaemia-reperfusion-induced pulmonary dysfunction is a significant clinical problem in cardiac surgery and, particularly, lung transplantation 1 . (ersjournals.com)
  • The redox-dependent regulation of protein function in the setting of ischaemia and reperfusion. (kcl.ac.uk)
  • Rossello X, Lobo-Gonzalez M and Ibanez B: Editor's choice-pathophysiology and therapy of myocardial ischaemia/reperfusion syndrome. (spandidos-publications.com)