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https://www.readbyqxmd.com/read/28534645/the-mitochondria-targeting-peptide-elamipretide-diminishes-circulating-htra2-in-st-segment-elevation-myocardial-infarction
#1
Marcus Hortmann, Samuel Robinson, Moritz Mohr, Maximillian Mauler, Daniela Stallmann, Jochen Reinöhl, Daniel Duerschmied, Karlheinz Peter, James Carr, C Michael Gibson, Christoph Bode, Ingo Ahrens
BACKGROUND: The extent of myocardial damage in patients with ST-segment elevation myocardial infarction (STEMI) depends on both the time to reperfusion as well as injury induced by ischaemia-reperfusion resulting in a cascade of cellular and humoral reactions. As a consequence of ischaemia-reperfusion in the heart, the high-temperature requirement serine peptidase 2 (HtrA2) is translocated from the mitochondria to the cytosol, whereupon it induces protease activity-dependent apoptosis mediated via caspases...
May 1, 2017: European Heart Journal. Acute Cardiovascular Care
https://www.readbyqxmd.com/read/28534140/protective-effects-of-neural-crest-derived-stem-cell-conditioned-media-against-ischemia-reperfusion-induced-lung-injury-in-rats
#2
Chung-Kan Peng, Shu-Yu Wu, Shih-En Tang, Min-Hui Li, Shih-Shiuan Lin, Shi-Jye Chu, Kun-Lun Huang
Current treatments for ischemia-reperfusion (IR)-induced acute lung injury are limited. Mesenchymal stem cell-conditioned medium (CM) has been reported to attenuate lung injury. Neural crest stem cells (NCSCs), a type of multipotent stem cells, are more easily obtained than mesenchymal stem cells. We hypothesize that NCSC-CM has anti-inflammatory properties that could protect against IR-induced lung injury in rats. In this study, NCSC-CM was derived from rat NCSCs. Typical acute lung injury was induced by 30-min ischemia followed by 90-min reperfusion in adult male Sprague-Dawley rats...
May 23, 2017: Inflammation
https://www.readbyqxmd.com/read/28534118/exercise-induced-circulating-extracellular-vesicles-protect-against-cardiac-ischemia-reperfusion-injury
#3
Yihua Bei, Tianzhao Xu, Dongchao Lv, Pujiao Yu, Jiahong Xu, Lin Che, Avash Das, John Tigges, Vassilios Toxavidis, Ionita Ghiran, Ravi Shah, Yongqin Li, Yuhui Zhang, Saumya Das, Junjie Xiao
Extracellular vesicles (EVs) serve an important function as mediators of intercellular communication. Exercise is protective for the heart, although the signaling mechanisms that mediate this cardioprotection have not been fully elucidated. Here using nano-flow cytometry, we found a rapid increase in plasma EVs in human subjects undergoing exercise stress testing. We subsequently identified that serum EVs were increased by ~1.85-fold in mice after 3-week swimming. Intramyocardial injection of equivalent quantities of EVs from exercised mice and non-exercised controls provided similar protective effects against acute ischemia/reperfusion (I/R) injury in mice...
July 2017: Basic Research in Cardiology
https://www.readbyqxmd.com/read/28533661/macrophage-inflammatory-protein-2-as-mediator-of-inflammation-in-acute-liver-injury
#4
REVIEW
Chao-Chao Qin, Yan-Ning Liu, Ying Hu, Ying Yang, Zhi Chen
Macrophage inflammatory protein (MIP)-2 is one of the CXC chemokines and is also known as chemokine CXC ligand (CXCL2). MIP-2 affects neutrophil recruitment and activation through the p38 mitogen-activated-protein-kinase-dependent signaling pathway, by binding to its specific receptors, CXCR1 and CXCR2. MIP-2 is produced by a variety of cell types, such as macrophages, monocytes, epithelial cells, and hepatocytes, in response to infection or injury. In liver injury, activated Kupffer cells are known as the major source of MIP-2...
May 7, 2017: World Journal of Gastroenterology: WJG
https://www.readbyqxmd.com/read/28533269/pharmacological-enrollment-of-aldehyde-dehydrogenase-modulators-to-assist-treating-ischemia-reperfusion-induced-intestinal-injury-is-there-a-gap-to-be-bridged
#5
Laurent Dollé
This commentary highlights the research presented by Zhu et al. [1]. In this issue of the Clinical Science, the authors evaluated the protective effect of Alda-1 (a novel class of small molecule aldehyde dehydrogenase (ALDH2) activators) in the intestinal ischemia reperfusion (IR) injury. Remarkably, enhancing the ADLH2 activity by the use of Alda-1 can ameliorate several deleterious effects related to aldehydes, and may provide a better protection against an injury preestablished by IR. Together, an innovative metabolic strategy for treating patients with IR injury could be the use of ALDH modulators in a near future...
June 1, 2017: Clinical Science (1979-)
https://www.readbyqxmd.com/read/28531921/hesperetin-post-treatment-prevents-rat-cardiomyocytes-from-hypoxia-reoxygenation-injury-in-vitro-via-activating-pi3k-akt-signaling-pathway
#6
Shangfei He, Xianbao Wang, Yongkang Zhong, Lu Tang, Ya Zhang, Yuanna Ling, Zhipeng Tan, Pingzhen Yang, Aihua Chen
Hesperidin (HES), a citrus fruit extract, has beneficial effects on various ischemia/reperfusion (I/R) models. Here, we investigated the possible positive effect of hesperetin (HPT), an active metabolite of HES, and identified the potential molecular mechanisms involved in cardiomyocytes H/R-induced injury. To construct the cardiomyocyte model of hypoxia/reoxygenation (H/R) injury, cultured neonatal rat cardiomyocytes were subjected to 3h of hypoxia followed by 3h of reoxygenation. Cell viability and apoptosis were detected...
May 16, 2017: Biomedicine & Pharmacotherapy, Biomédecine & Pharmacothérapie
https://www.readbyqxmd.com/read/28531112/effects-of-polyphenols-on-oxidative-stress-mediated-injury-in-cardiomyocytes
#7
REVIEW
Rosanna Mattera, Monica Benvenuto, Maria Gabriella Giganti, Ilaria Tresoldi, Francesca Romana Pluchinotta, Sonia Bergante, Guido Tettamanti, Laura Masuelli, Vittorio Manzari, Andrea Modesti, Roberto Bei
Cardiovascular diseases are the main cause of mortality and morbidity in the world. Hypertension, ischemia/reperfusion, diabetes and anti-cancer drugs contribute to heart failure through oxidative and nitrosative stresses which cause cardiomyocytes nuclear and mitochondrial DNA damage, denaturation of intracellular proteins, lipid peroxidation and inflammation. Oxidative or nitrosative stress-mediated injury lead to cardiomyocytes apoptosis or necrosis. The reactive oxygen (ROS) and nitrogen species (RNS) concentration is dependent on their production and on the expression and activity of anti-oxidant enzymes...
May 20, 2017: Nutrients
https://www.readbyqxmd.com/read/28529484/targeting-adenosine-receptors-for-the-treatment-of-cardiac-fibrosis
#8
REVIEW
Elizabeth A Vecchio, Paul J White, Lauren T May
Adenosine is a ubiquitous molecule with key regulatory and cytoprotective mechanisms at times of metabolic imbalance in the body. Among a plethora of physiological actions, adenosine has an important role in attenuating ischaemia-reperfusion injury and modulating the ensuing fibrosis and tissue remodeling following myocardial damage. Adenosine exerts these actions through interaction with four adenosine G protein-coupled receptors expressed in the heart. The adenosine A2B receptor (A2BAR) is the most abundant adenosine receptor (AR) in cardiac fibroblasts and is largely responsible for the influence of adenosine on cardiac fibrosis...
2017: Frontiers in Pharmacology
https://www.readbyqxmd.com/read/28528966/nampt-inhibitor-protects-ischemic-neuronal-injury-in-rat-brain-via-anti-neuroinflammation
#9
Chen-Xiang Chen, Jing Huang, Ga-Qi Tu, Jia-Tong Lu, Xian Xie, Bing Zhao, Ming Wu, Qiao-Juan Shi, San-Hua Fang, Er-Qing Wei, Wei-Ping Zhang, Yun-Bi Lu
Nicotinamide phosphoribosyltransferase (NAMPT) is an important neuroprotective factor in cerebral ischemia, and it has been reported that NAMPT inhibitors can aggravate neuronal injury in the acute phase. However, because it is a cytokine, NAMPT participates in many inflammatory diseases in the peripheral system, and its inhibitors have therapeutic effects. Following cerebral ischemia, the peripheral and resident inflammatory and immune cells produce many pro-inflammatory mediators in the ischemic area, which induce neuroinflammation and impair the brain...
May 18, 2017: Neuroscience
https://www.readbyqxmd.com/read/28527782/protective-roles-of-bioactive-peptides-during-ischemia-reperfusion-injury-from-bench-to-bedside
#10
REVIEW
Dongdong Wu, Jun Wang, Honggang Wang, Ailing Ji, Yanzhang Li
Ischemia-reperfusion (I/R) is a well-known pathological condition which may lead to disability and mortality. I/R injury remains an unresolved and complicated situation in a number of clinical conditions, such as cardiac arrest with successful reanimation, as well as ischemic events in brain and heart. Peptides have many attractive advantages which make them suitable candidate drugs in treating I/R injury, such as low toxicity and immunogenicity, good solubility property, distinct tissue distribution pattern, and favorable pharmacokinetic profile...
May 17, 2017: Life Sciences
https://www.readbyqxmd.com/read/28526762/exacerbation-of-thromboinflammation-by-hyperglycemia-precipitates-cerebral-infarct-growth-and-hemorrhagic-transformation
#11
Jean-Philippe Desilles, Varouna Syvannarath, Véronique Ollivier, Clément Journé, Sandrine Delbosc, Célina Ducroux, William Boisseau, Liliane Louedec, Lucas Di Meglio, Stéphane Loyau, Martine Jandrot-Perrus, Louis Potier, Jean-Baptiste Michel, Mikael Mazighi, Benoit Ho-Tin-Noé
BACKGROUND AND PURPOSE: Admission hyperglycemia is associated with a poor outcome in acute ischemic stroke. How hyperglycemia impacts the pathophysiology of acute ischemic stroke remains largely unknown. We investigated how preexisting hyperglycemia increases ischemia/reperfusion cerebral injury. METHODS: Normoglycemic and streptozotocin-treated hyperglycemic rats were subjected to transient middle cerebral artery occlusion. Infarct growth and brain perfusion were assessed by magnetic resonance imaging...
May 19, 2017: Stroke; a Journal of Cerebral Circulation
https://www.readbyqxmd.com/read/28526717/major-contribution-of-the-3-6-7-class-of-trpc-channels-to-myocardial-ischemia-reperfusion-and-cellular-hypoxia-reoxygenation-injuries
#12
Xiju He, Shoutian Li, Benju Liu, Sebastian Susperreguy, Karina Formoso, Jinghong Yao, Jinsong Kang, Anbing Shi, Lutz Birnbaumer, Yanhong Liao
The injury phase after myocardial infarcts occurs during reperfusion and is a consequence of calcium release from internal stores combined with calcium entry, leading to cell death by apoptopic and necrotic processes. The mechanism(s) by which calcium enters cells has(ve) not been identified. Here, we identify canonical transient receptor potential channels (TRPC) 3 and 6 as the cation channels through which most of the damaging calcium enters cells to trigger their death, and we describe mechanisms activated during the injury phase...
May 19, 2017: Proceedings of the National Academy of Sciences of the United States of America
https://www.readbyqxmd.com/read/28525945/the-protective-effect-of-luteolin-on-myocardial-ischemia-reperfusion-i-r-injury-through-tlr4-nf-%C3%AE%C2%BAb-nlrp3-inflammasome-pathway
#13
Xu Zhang, Qianming Du, Yan Yang, Jianing Wang, Shuai Dou, Chao Liu, Junguo Duan
The purpose of the present study was to investigate the effect of Luteolin(Lut) on myocardial ischemia reperfusion injury and explore the underlying mechanism. Myocardial ischemia reperfusion injury (I/R) model was induced with 30min of left anterior descending (LAD) occlusion followed by 24h of reperfusion. In vivo, the rats were randomly divided into 5 groups: (1)Sham, (2)I/R, (3)I/R+Lut(40mg/kg), (4)I/R+Lut(80mg/kg) and (5)I/R+Lut(160mg/kg). In vitro, the H9c2 cells were assigned to five groups: (1)control, (2)hypoxia-reoxygenation(H/R), (3)H/R+Lut(5μM), (4)H/R+Lut(10μM) and (5)H/R+Lut(20μM)...
May 15, 2017: Biomedicine & Pharmacotherapy, Biomédecine & Pharmacothérapie
https://www.readbyqxmd.com/read/28525795/the-role-of-secretory-phospholipases-as-therapeutic-targets-for-the-treatment-of-myocardial-ischemia-reperfusion-injury
#14
REVIEW
Sriram Ravindran, Gino A Kurian
Myocardial reperfusion injury is a consequence of restoration of blood flow post ischemia. It is a complex process involving an acute inflammatory response activated by cytokines, chemokines, growth factors, and mediated by free radicals, calcium overload leading to mitochondrial dysfunction. Secretory phospholipases (sPLA2) are a group of pro-inflammatory molecules associated with diseases such as atherosclerosis, which increase the risk of reperfusion injury. This acute response leads to breakdown of phospholipids such as cardiolipin, found in the mitochondrial inner membrane, leading to disruption of energy producing enzymes of the electron transport chain...
May 16, 2017: Biomedicine & Pharmacotherapy, Biomédecine & Pharmacothérapie
https://www.readbyqxmd.com/read/28525507/subcellular-energetics-and-metabolism-a-cross-species-framework
#15
Robert H Thiele
Although it is generally believed that oxidative phosphorylation and adequate oxygenation are essential for life, human development occurs in a profoundly hypoxic environment and "normal" levels of oxygen during embryogenesis are even harmful. The ability of embryos not only to survive but also to thrive in such an environment is made possible by adaptations related to metabolic pathways. Similarly, cancerous cells are able not only to survive but also to grow and spread in environments that would typically be fatal for healthy adult cells...
June 2017: Anesthesia and Analgesia
https://www.readbyqxmd.com/read/28524859/mesenchymal-stem-cells-sense-mitochondria-released-from-damaged-cells-as-danger-signals-to-activate-their-rescue-properties
#16
Meriem Mahrouf-Yorgov, Lionel Augeul, Claire Crola Da Silva, Maud Jourdan, Muriel Rigolet, Sylvie Manin, René Ferrera, Michel Ovize, Adeline Henry, Aurélie Guguin, Jean-Paul Meningaud, Jean-Luc Dubois-Randé, Roberto Motterlini, Roberta Foresti, Anne-Marie Rodriguez
Mesenchymal stem cells (MSCs) protect tissues against cell death induced by ischemia/reperfusion insults. This therapeutic effect seems to be controlled by physiological cues released by the local microenvironment following injury. Recent lines of evidence indicate that MSC can communicate with their microenvironment through bidirectional exchanges of mitochondria. In particular, in vitro and in vivo studies report that MSCs rescue injured cells through delivery of their own mitochondria. However, the role of mitochondria conveyed from somatic cells to MSC remains unknown...
May 19, 2017: Cell Death and Differentiation
https://www.readbyqxmd.com/read/28524210/sulfur-dioxide-foe-or-friend-for-life
#17
REVIEW
Xin-Bao Wang, Hong Cui, Xiaohong Liu, Jun-Bao Du
Sulfur dioxide (SO₂) is a toxic gas and air pollutant. The toxic effects of SO₂ have been extensively studied. Oxidative damage due to SO2 can occur in multiple organs. Inhaled SO₂ can also cause chromosomal aberrations, DNA damage and gene mutations in mammals. However, SO₂ can also be generated from the sulfur-containing amino acid, L-cysteine. Recent studies have shown that SO₂ has a vasorelaxant effect, and ameliorates pulmonary hypertension and vascular remodeling. SO₂ can also reduce lung injury and myocardial injury in rats...
May 19, 2017: Histology and Histopathology
https://www.readbyqxmd.com/read/28522565/integrin-%C3%AE-v%C3%AE-5-inhibition-protects-against-ischemia-reperfusion-induced-lung-injury-in-an-autophagy-dependent-manner
#18
Dan Zhang, Chichi Li, Yuanlin Song, Jian Zhou, Yuping Li, Jing Li, Chunxue Bai
Integrin αvβ5 mediates pulmonary endothelial barrier function and acute lung injury (LI), but its roles in cell apoptosis and autophagy are unclear. Thus, the aims of this study were to investigate the significance of αvβ5 in ischemia/reperfusion (I/R)-induced apoptosis and LI and to explore the relationship between αvβ5 and autophagy. Human pulmonary micro-vascular endothelial cells (HPMVECs) were pretreated with an αvβ5-blocking antibody (ALULA) and challenged with oxygen-glucose deprivation/oxygen-glucose restoration, which mimics I/R; then, cellular autophagy and apoptosis were detected, and cell permeability was assessed...
May 18, 2017: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/28522550/suppression-of-microrna-135b-5pprotects-againstmyocardial-ischemia-reperfusion-injury-by-activatingjak2-stat3-signaling-pathway-in-mice-duringsevofluraneanesthesia
#19
Xiao-Juan Xie, Dong-Mei Fan, Kai Xi, Ya-Wei Chen, Peng-Wei Qi, Qian-Hui Li, Liang Fang, Li-Gang Ma
The study aims to explore the effects of miR-135b-5p on myocardial ischemia/reperfusion (I/R) injuries by regulating JAK2/STAT signaling pathway by mediating inhalation anesthesia with sevoflurane. A sum of 120 healthy Wistar male mice was assigned into six groups. Left ventricular ejection fraction (LVEF) and left ventricular shortening fraction (LVSF) were detected. Cardiomyocyte apoptosis was determined by TUNEL assay. MiR-135b-5p expression, mRNA and protein expression of p-STAT3, p-JAK2, STAT3, JAK2, Bcl2 and Bax were detected by qRT-PCR and Western blotting...
May 18, 2017: Bioscience Reports
https://www.readbyqxmd.com/read/28522336/geldanamycin-inhibits-fas-signaling-pathway-and-protects-neurons-against-ischemia
#20
Xiao-Hui Yin, Yan-Ling Han, Ying Zhuang, Jing-Zhi Yan, Chong Li
The inhibitor of Heat shock proteins 90, geldanamycin (GA), has been reported neuroprotective against both global and focal brain ischemia. To understand the mechanisms underlies the neuroprotection effect of GA, we investigated the relationship between GA pretreatment and Fas signaling pathway in rat global brain ischemia/reperfusion model in the present study. Results showed that GA attenuated neuron loss significantly in hippocampal CA1 region. Upon GA pretreatment, Mixed Lineage Kinase 3 (MLK3) expression and activation and FasL expression was decreased, the assembly of death-inducing signaling complex and activation of downstream apoptosis-associating proteins were inhibited along with neuroprotection...
May 15, 2017: Neuroscience Research
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