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myocardial reperfusion injury

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https://www.readbyqxmd.com/read/28444132/tyrosine-phosphorylation-of-enos-regulates-myocardial-survival-after-an-ischaemic-insult-role-of-pyk2
#1
Sofia-Iris Bibli, Zongmin Zhou, Sven Zukunft, Beate Fisslthaler, Ioanna Andreadou, Csaba Szabo, Peter Brouckaert, Ingrid Fleming, Andreas Papapetropoulos
Aims: Endothelial nitric oxide (NO) synthase (eNOS) is known to play a cardioprotective protective. However, the molecular mechanisms regulating eNOS activity during ischaemia/reperfusion (I/R) injury are incompletely understood. eNOS is a substrate for several kinases that positively or negatively affect its enzymatic activity. Herein, we sought to correlate eNOS phosphorylation status with cardiomyocyte survival and we investigated the contribution of the proline-rich tyrosine kinase 2 (PYK2)/eNOS axis to the regulation of myocardial infarct size in vivo...
April 20, 2017: Cardiovascular Research
https://www.readbyqxmd.com/read/28444063/effect-of-lactation-on-myocardial-vulnerability-to-ischemic-insult-in-rats
#2
Sahar Askari, Alireza Imani, Hamidreza Sadeghipour, Mahdieh Faghihi, Zohreh Edalatyzadeh, Samira Choopani, Nasser Karimi, Sulail Fatima
Background: Cardiovascular diseases are the leading cause of mortality and long-term disability worldwide. Various studies have suggested a protective effect of lactation in reducing the risk of cardiovascular diseases. Objective: This study was designed to assess the effects of pregnancy and lactation on the vulnerability of the myocardium to an ischemic insult. Methods: Eighteen female rats were randomly divided into three groups: ischemia-reperfusion (IR), in which the hearts of virgin rats underwent IR (n = 6); lactating, in which the rats nursed their pups for 3 weeks and the maternal hearts were then submitted to IR (n = 6); and non-lactating, in which the pups were separated after birth and the maternal hearts were submitted to IR (n = 6)...
April 20, 2017: Arquivos Brasileiros de Cardiologia
https://www.readbyqxmd.com/read/28442910/targeted-delivery-of-thymosin-beta-4-to-the-injured-myocardium-using-creka-conjugated-nanoparticles
#3
Zheyong Huang, Yanan Song, Zhiqing Pang, Bo Zhang, Hongbo Yang, Hongtao Shi, Jing Chen, Hui Gong, Juying Qian, Junbo Ge
PURPOSE: Thymosin beta 4 (Tβ4) has multiple beneficial facets for myocardial injury, but its efficiency is limited by the low local concentration within the infarct. Here, we established a Tβ4 delivery system for cardiac repair based on the interaction between the abundant fibrin in the infarct zone and the fibrin-targeting moiety clot-binding peptide cysteine-arginine-glutamic acid-lysine-alanine (CREKA). METHODS AND RESULTS: CREKA and Tβ4 were conjugated to nanoparticles (CNP-Tβ4)...
2017: International Journal of Nanomedicine
https://www.readbyqxmd.com/read/28442264/mitochondrial-lon-protease-dependent-degradation-of-cytochrome-c-oxidase-subunits-under-hypoxia-and-myocardial-ischemia
#4
Naresh B V Sepuri, Rajesh Angireddy, Satish Srinivasan, Manti Guha, Joseph Spear, Bin Lu, Hindupur K Anandatheerthavarada, Carolyn K Suzuki, Narayan G Avadhani
The mitochondrial ATP dependent matrix protease, Lon, is involved in the maintenance of mitochondrial DNA nucleoids and degradation of abnormal or misfolded proteins. The Lon protease regulates mitochondrial Tfam (mitochondrial transcription factor A) level and thus modulates mitochondrial DNA (mtDNA) content. We have previously shown that hypoxic stress induces the PKA-dependent phosphorylation of cytochrome c oxidase (CcO) subunits I, IVi1, and Vb and a time-dependent reduction of these subunits in RAW 264...
April 22, 2017: Biochimica et Biophysica Acta
https://www.readbyqxmd.com/read/28440739/featured-article-pharmacological-postconditioning-with-delta-opioid-attenuates-myocardial-reperfusion-injury-in-isolated-porcine-hearts
#5
Maria Seewald, James A Coles, Daniel C Sigg, Paul A Iaizzo
Ischemic preconditioning has been utilized to protect the heart from ischemia prior to ischemia onset, whereas postconditioning is employed to minimize the consequences of ischemia at the onset of reperfusion. The underlying mechanisms and pathways of ischemic pre- and postconditioning continue to be investigated as therapeutic targets. We evaluated the administration of a delta opioid agonist or cariporide on various parameters associated with myocardial reperfusion injury upon reperfusion of isolated porcine hearts...
May 2017: Experimental Biology and Medicine
https://www.readbyqxmd.com/read/28440490/microrna-15a-inhibition-protects-against-hypoxia-reoxygenation-induced-apoptosis-of-cardiomyocytes-by-targeting-mothers-against-decapentaplegic-homolog-7
#6
Yang Yang, Shiao Ding, Gaojun Xu, Fei Chen, Fangbao Ding
Myocardial ischemia/reperfusion (I/R) injury is a major pathological process in coronary heart disease and cardiac surgery, and is associated with aberrant microRNA (miR) expression. Previous studies have demonstrated that inhibition of miR-15a expression may ameliorate I/R‑induced myocardial injury. In the present study, the potential role and underlying mechanism of miR‑15a in hypoxia/reoxygenation‑induced apoptosis of cardiomyocytes was investigated. Myocardial I/R was simulated in cultured H9c2 cells by 24 h hypoxia followed by 24 h reoxygenation...
April 12, 2017: Molecular Medicine Reports
https://www.readbyqxmd.com/read/28438640/neutralizing-il-6-reduces-heart-injury-by-decreasing-nerve-growth-factor-precursor-in-the-heart-and-hypothalamus-during-rat-cardiopulmonary-bypass
#7
Chi Cheng, Jun-Mei Xu, Tian Yu
AIMS: To investigate whether the expression of nerve growth factor precursor (proNGF) changes during cardiopulmonary bypass (CPB) and whether neutralizing interleukin-6 (IL-6) during CPB has cardiac benefits. MAIN METHODS: Thirty patients undergoing CPB were recruited and their serum proNGF and troponin-I (TNI) were detected. In addition, rats were divided into three groups: CPB group, CPB with cardiac ischemia-reperfusion (IR) group, and a control group. The pre-CPB standard deviation of N-N intervals (SDNN) and post-CPB SDNN were compared...
April 21, 2017: Life Sciences
https://www.readbyqxmd.com/read/28433557/early-changes-of-left-ventricular-filling-pattern-after-reperfused-st-elevation-myocardial-infarction-and-doxycycline-therapy-insights-from-the-tiptop-trial
#8
Giampaolo Cerisano, Piergiovanni Buonamici, Guido Parodi, Alberto Santini, Guia Moschi, Renato Valenti, Angela Migliorini, Paolo Colonna, Benedetta Bellandi, Anna Maria Gori, David Antoniucci
AIM: Metalloproteinases inhibition by doxycycline reduces cardiac protein degradation at extracellular and intracellular level in the experimental model ischemia/reperfusion injury. Since both extracellular cardiac matrix and titin filaments inside the cardiomyocyte are responsible for the myocardial stiffness, we hypothesized that doxycycline could favorably act on left ventricular (LV) filling pressures in patients after reperfused acute ST-elevation myocardial infarction (STEMI). METHODS AND RESULTS: Seventy-three of 110 patients of the TIPTOP trial underwent a 2D-Echo-Doppler on admission, and at pre-discharge and at 6-month after a primary PCI for STEMI and LV dysfunction...
April 7, 2017: International Journal of Cardiology
https://www.readbyqxmd.com/read/28432149/cd73-on-t-cells-orchestrates-cardiac-wound-healing-after-myocardial-infarction-by-purinergic-metabolic-reprogramming
#9
Nadine Borg, Christina Alter, Nicole Görldt, Christoph Jacoby, Zhaoping Ding, Bodo Steckel, Christine Quast, Florian Bönner, Daniela Friebe, Sebastian Temme, Ulrich Flögel, Jürgen Schrader
Background -T-cells are required for proper healing after myocardial infarction. The mechanism of their beneficial action, however, is unknown. The pro-inflammatory "danger signal" adenosine triphosphate (ATP), released from damaged cells, is degraded by the ectonucleotidases CD39 and CD73 to the anti-inflammatory mediator adenosine. Here, we investigate the contribution of CD73-derived adenosine produced by T-cells to cardiac remodeling after ischemia/reperfusion and define its mechanism of action. Methods -Myocardial ischemia (50 min /reperfusion) was induced in global CD73(-/-) and CD4-CD73(-/-) mice...
April 21, 2017: Circulation
https://www.readbyqxmd.com/read/28432060/toll-like-receptor-2-tlr2-dominance-over-tlr4-in-stressful-conditions-for-its-detrimental-role-in-the-heart
#10
Ashim K Bagchi, Gauri Akolkar, Soma Mandal, Prathapan Ayyappan, Xi Yang, Pawan K Singal
It has been suggested that toll-like receptor 4 (TLR4) promotes interleukin-10 (IL-10)-mediated cardiac cell survival while another receptor, TLR2, from the same family is detrimental. Here we examined the interactive role of these two innate signaling molecules under stressful conditions including interleukin-10 knockout (IL-10(-/-)) mice, global ischemia/reperfusion (I/R) injury in rat hearts and in-vitro shRNA experimental models in presence or absence of IL-10 (10ng/ml). Circulating and myocardial levels of tumor necrosis factor-α (TNF-α) as well as apoptosis and fibrosis were higher in IL-10(-/-) mice...
April 21, 2017: American Journal of Physiology. Heart and Circulatory Physiology
https://www.readbyqxmd.com/read/28429857/ndufa4l2-protects-against-ischemia-reperfusion-induced-cardiomyocyte-apoptosis-and-mitochondrial-dysfunction-by-inhibiting-complex-i
#11
Jianhua Li, Caiyan Bai, Junxia Guo, Wanqian Liang, Jingning Long
Myocardial ischemia/reperfusion (I/R) injury may cause the apoptosis of cardiomyocytes as well as mitochondrial dysfunction. The aims of the present study were to investigate whether NADH dehydrogenase 1 alpha subcomplex subunit 4-like 2 (NDUFA4L2) on myocardial ischemia-reperfusion (I/R) injury and the underlying molecular mechanism. The hypoxia-reperfusion (H/R) model was established in vitro using H9c2 cells to simulate I/R injury. NDUFA4L2 and complex I expression levels were detected using RT-PCR and western blot...
April 21, 2017: Clinical and Experimental Pharmacology & Physiology
https://www.readbyqxmd.com/read/28429351/tgf%C3%AE-1-protects-myocardium-from-apoptosis-and-oxidative-damage-after-ischemia-reperfusion
#12
Y-F Liu, Y-Y Chu, X-Z Zhang, M Zhang, F-G Xie, M Zhou, H-H Wen, A-H Shu
OBJECTIVE: Myocardial apoptosis is an important pathologic basis of ischemia-reperfusion injury (I/R). Transforming growth factor β1 (TGFβ1) participates in the regulation of oxidative damage and apoptosis. TGFβ1 is upregulated in the repair process of I/R injury. It is speculated that TGFβ1 over-expression is involved in the endogenous protective mechanism of I/R injury. This study explores the significance of TGFβ1 in myocardial cell apoptosis after I/R. MATERIALS AND METHODS: Rat myocardial I/R injury model was established...
April 2017: European Review for Medical and Pharmacological Sciences
https://www.readbyqxmd.com/read/28424623/notch-signaling-in-ischemic-damage-and-fibrosis-evidence-and-clues-from-the-heart
#13
REVIEW
Silvia Nistri, Chiara Sassoli, Daniele Bani
Notch signaling is a major intercellular coordination mechanism highly conserved throughout evolution. In vertebrates, Notch signaling is physiologically involved in embryo development, including mesenchymal cell commitment, formation of heart tissues and angiogenesis. In post-natal life, Notch signaling is maintained as a key mechanism of cell-cell communication and its dysregulations have been found in pathological conditions such as ischemic and fibrotic diseases. In the heart, Notch takes part in the protective response to ischemia, being involved in pre- and post-conditioning, reduction of reperfusion-induced oxidative stress and myocardial damage, and cardiomyogenesis...
2017: Frontiers in Pharmacology
https://www.readbyqxmd.com/read/28421373/role-of-glycogen-synthase-kinase-following-myocardial-infarction-and-ischemia-reperfusion
#14
REVIEW
S Ghaderi, N Alidadiani, N Dilaver, H R Heidari, R Parvizi, R Rahbarghazi, J Soleimani-Rad, B Baradaran
Glycogen synthase kinase-3 beta (GSK3β) is principally is a glycogen synthase phosphorylating enzyme that is well known for its role in muscle metabolism. GSK3β is a serine/threonine protein Kinase, which is responsible for several essential roles in mammalian cells. This enzyme is implicated in the pathophysiology of many conditions involved in homeostasis and cellular immigration. GSK3β is involved in several pathways leading to neurodegenerative diseases such as Alzheimer's disease and Parkinson's disease...
April 18, 2017: Apoptosis: An International Journal on Programmed Cell Death
https://www.readbyqxmd.com/read/28420993/phellinus-linteus-mycelium-alleviates-myocardial-ischemia-reperfusion-injury-through-autophagic-regulation
#15
Hsing-Hui Su, Ya-Chun Chu, Jiuan-Miaw Liao, Yi-Hsin Wang, Ming-Shiou Jan, Chia-Wei Lin, Chiu-Yeh Wu, Chin-Yin Tseng, Jiin-Cherng Yen, Shiang-Suo Huang
The incidence of myocardial ischemia-reperfusion (IR) injury is rapidly increasing around the world and this disease is a major contributor to global morbidity and mortality. It is known that regulation of programmed cell death including apoptosis and autophagy reduces the impact of myocardial IR injury. In this study, the cardioprotective effects and underlying mechanisms of Phellinus linteus (Berk. and Curt.) Teng, Hymenochaetaceae (PL), a type of medicinal mushroom, were examined in rats subjected to myocardial IR injury...
2017: Frontiers in Pharmacology
https://www.readbyqxmd.com/read/28416795/neutrophil-stunning-by-metoprolol-reduces-infarct-size
#16
Jaime García-Prieto, Rocío Villena-Gutiérrez, Mónica Gómez, Esther Bernardo, Andrés Pun-García, Inés García-Lunar, Georgiana Crainiciuc, Rodrigo Fernández-Jiménez, Vinatha Sreeramkumar, Rafael Bourio-Martínez, José M García-Ruiz, Alfonso Serrano Del Valle, David Sanz-Rosa, Gonzalo Pizarro, Antonio Fernández-Ortiz, Andrés Hidalgo, Valentín Fuster, Borja Ibanez
The β1-adrenergic-receptor (ADRB1) antagonist metoprolol reduces infarct size in acute myocardial infarction (AMI) patients. The prevailing view has been that metoprolol acts mainly on cardiomyocytes. Here, we demonstrate that metoprolol reduces reperfusion injury by targeting the haematopoietic compartment. Metoprolol inhibits neutrophil migration in an ADRB1-dependent manner. Metoprolol acts during early phases of neutrophil recruitment by impairing structural and functional rearrangements needed for productive engagement of circulating platelets, resulting in erratic intravascular dynamics and blunted inflammation...
April 18, 2017: Nature Communications
https://www.readbyqxmd.com/read/28409534/bifidobacterium-animalis-subsp-lactis-420-mitigates-the-pathological-impact-of-myocardial-infarction-in-the-mouse
#17
C A Danilo, E Constantopoulos, L A McKee, H Chen, J A Regan, Y Lipovka, S Lahtinen, L K Stenman, T-V V Nguyen, K P Doyle, M J Slepian, Z I Khalpey, J P Konhilas
There is a growing appreciation that our microbial environment in the gut plays a critical role in the maintenance of health and the pathogenesis of disease. Probiotic, beneficial gut microbes, administration can directly attenuate cardiac injury and post-myocardial infarction (MI) remodelling, yet the mechanisms of cardioprotection are unknown. We hypothesised that administration of Bifidobacterium animalis subsp. lactis 420 (B420), a probiotic with known anti-inflammatory properties, to mice will mitigate the pathological impact of MI, and that anti-inflammatory T regulatory (Treg) immune cells are necessary to impart protection against MI as a result of B420 administration...
April 14, 2017: Beneficial Microbes
https://www.readbyqxmd.com/read/28407045/novel-pathogenesis-regulation-of-apoptosis-by-apelin-apj-system
#18
Jiaqi Liu, Meiqing Liu, Linxi Chen
Apelin is the endogenous peptide APJ receptor, while APJ is a member of the G protein-coupled receptors family. Recent evidence strongly suggests that Apelin/APJ system influences apoptosis in various diseases through different signal pathways. In this review, we discuss the possible mechanisms by which the Apelin/APJ system inhibits apoptosis, including the phosphatidylinositol-3-kinase (PI3K)/Akt, ERK1/2, caspase signaling, and autophagy pathway. We also summarize the role of Apelin/APJ system in apoptosis in myocardial ischemia-reperfusion (I/R) injury, pulmonary artery hypertension, retinal neovascular disease, acute renal injury, skeletal homeostasis, and gastrointestinal diseases...
April 12, 2017: Acta Biochimica et Biophysica Sinica
https://www.readbyqxmd.com/read/28406705/tolerance-of-isolated-rabbit-hearts-to-short-ischemic-periods-is-affected-by-increased-lv-mass-fraction
#19
M Hlaváčová, V Olejníčková, M Ronzhina, T Stračina, O Janoušek, M Nováková, P Babula, J Kolářová, I Provazník, H Paulová
Hypertrophied hearts are known for increased risk of arrhythmias and are linked with reduced ischemic tolerance. However, still little is known about state characterized only by increased left ventricle (LV) mass fraction. Seventeen isolated rabbit hearts with various LV mass were divided into two groups according to LV weight/heart weight ratio (LVW/HW ratio), namely group H and L (with higher and lower LVW/HW ratio, respectively) and underwent three short cycles of global ischemia and reperfusion. The differences in electrogram (heart rate, QRS(max), mean number, onset and dominant form of ventricular premature beats) and in biochemical markers of myocardial injury (creatine kinase, lactate dehydrogenase - LDH) and lipid peroxidation (4-hydroxy-2-nonenal - 4-HNE) were studied...
April 12, 2017: Physiological Research
https://www.readbyqxmd.com/read/28404768/dj-1-overexpression-restores-ischaemic-post-conditioning-mediated-cardioprotection-in-diabetic-rats-%C3%AF-role-of-autophagy
#20
Bin Zhou, Shaoqing Lei, Rui Xue, Yan Leng, Zhengyuan Xia, Zhong-Yuan Xia
IPO (Ischaemic post-conditioning) is a promising method of alleviating myocardial IR (ischaemia -reperfusion) injury; however, IPO-mediated cardioprotection is lost in diabetic hearts via mechanisms that remain largely unclear. We hypothesized that decreased cardiac expression of DJ-1, a positive modulator of autophagy, compromises the effectiveness of IPO-induced cardioprotection in diabetic rats. Diabetic rats subjected to myocardial IR (30 min of coronary artery occlusion followed by 120 min of reperfusion) exhibited more severe myocardial injury, less cardiac autophagy, lower DJ-1 expression and AMPK (adenosine monophosphate-activated protein kinase)/mTOR (mammalian target of rapamycin) pathway activity than non-diabetic rats...
April 12, 2017: Clinical Science (1979-)
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