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heart and ischemia and mitochondria

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https://www.readbyqxmd.com/read/28421373/role-of-glycogen-synthase-kinase-following-myocardial-infarction-and-ischemia-reperfusion
#1
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/28413502/remifentanil-functions-in-the-adaptive-protection-of-cardiac-function-following-ischemia
#2
Jie Hou, Huishan Wang, Xinmin Li, Yan Zhu
The present study aimed to investigate the effects of remifentanil during adaptation followinsg myocardial ischemia, and its possible clinical applications. Remifentanil was used during the simulation of adaptation following ischemia, which was performed using a Langendorff heart perfusion system. A total of 75 rats were divided into five groups, and the coronary flow, cardiac output and the cardiac enzyme content in coronary effluent prior to ischemia and post-reperfusion were recorded. Electron microscopy was used to observe myocardial ultrastructure, and the volume of aortic and coronary effluent was also measured...
April 2017: Experimental and Therapeutic Medicine
https://www.readbyqxmd.com/read/28408349/early-effects-of-prolonged-cardiac-arrest-and-ischemic-postconditioning-during-cardiopulmonary-resuscitation-on-cardiac-and-brain-mitochondrial-function-in-pigs
#3
Timothy R Matsuura, Jason A Bartos, Adamantios Tsangaris, Kadambari Chandra Shekar, Matthew D Olson, Matthias L Riess, Martin Bienengraeber, Tom P Aufderheide, Robert W Neumar, Jennifer N Rees, Scott H McKnite, Anna E Dikalova, Sergey I Dikalov, Hunter F Douglas, Demetris Yannopoulos
Background Out-of-hospital cardiac arrest (CA) is a prevalent medical crisis resulting in severe injury to the heart and brain and an overall survival of less than 10 percent. Mitochondrial dysfunction is predicted to be a key determinant of poor outcomes following prolonged CA. However, the onset and severity of mitochondrial dysfunction during CA and cardiopulmonary resuscitation (CPR) is not fully understood. Ischemic postconditioning (IPC), controlled pauses during the initiation of CPR, has been shown to improve cardiac function and neurologically favorable outcomes after fifteen minutes of CA...
April 10, 2017: Resuscitation
https://www.readbyqxmd.com/read/28364353/mitochondrial-cx43-hemichannels-contribute-to-mitochondrial-calcium-entry-and-cell-death-in-the-heart
#4
Ashish Kumar Gadicherla, Nan Wang, Marco Bulic, Esperanza Agullo-Pascual, Alessio Lissoni, Maarten De Smet, Mario Delmar, Geert Bultynck, Dmitri V Krysko, Amadou Camara, Klaus-Dieter Schlüter, Rainer Schulz, Wai-Meng Kwok, Luc Leybaert
Mitochondrial connexin 43 (Cx43) plays a key role in cardiac cytoprotection caused by repeated exposure to short periods of non-lethal ischemia/reperfusion, a condition known as ischemic preconditioning. Cx43 also forms calcium (Ca(2+))-permeable hemichannels that may potentially lead to mitochondrial Ca(2+) overload and cell death. Here, we studied the role of Cx43 in facilitating mitochondrial Ca(2+) entry and investigated its downstream consequences. To that purpose, we used various connexin-targeting peptides interacting with extracellular (Gap26) and intracellular (Gap19, RRNYRRNY) Cx43 domains, and tested their effect on mitochondrial dye- and Ca(2+)-uptake, electrophysiological properties of plasmalemmal and mitochondrial Cx43 channels, and cell injury/cell death...
May 2017: Basic Research in Cardiology
https://www.readbyqxmd.com/read/28361886/enzyme-dependent-fluorescence-recovery-of-nadh-after-photobleaching-to-assess-dehydrogenase-activity-of-isolated-perfused-hearts
#5
Angel Moreno, Sarah Kuzmiak-Glancy, Rafael Jaimes, Matthew W Kay
Reduction of NAD(+) by dehydrogenase enzymes to form NADH is a key component of cellular metabolism. In cellular preparations and isolated mitochondria suspensions, enzyme-dependent fluorescence recovery after photobleaching (ED-FRAP) of NADH has been shown to be an effective approach for measuring the rate of NADH production to assess dehydrogenase enzyme activity. Our objective was to demonstrate how dehydrogenase activity could be assessed within the myocardium of perfused hearts using NADH ED-FRAP. This was accomplished using a combination of high intensity UV pulses to photobleach epicardial NADH...
March 31, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28360350/myocardial-viability-survival-mechanisms-and-molecular-imaging-targets-in-acute-and-chronic-ischemia
#6
REVIEW
Henry Gewirtz, Vasken Dilsizian
Myocardial responses to acute ischemia/reperfusion and to chronic ischemic conditions have been studied extensively at all levels of organization. These include subcellular (eg, mitochondria in vitro); intact, large animal models (eg, swine with chronic coronary stenosis); as well as human subjects. Investigations in humans have used positron emission tomographic metabolic and myocardial blood flow measurements, assessment of gene expression and anatomic description of myocardium obtained at the time of coronary artery revascularization, ventricular assist device placement, or heart transplantation...
March 31, 2017: Circulation Research
https://www.readbyqxmd.com/read/28352158/cardioprotection-with-halogenated-gases-how-does-it-occur
#7
REVIEW
Jose Luis Guerrero-Orriach, Juan Jose Escalona Belmonte, Alicia Ramirez Fernandez, Marta Ramirez Aliaga, Manuel Rubio Navarro, Jose Cruz Mañas
Numerous studies have studied the effect of halogenated agents on the myocardium, highlighting the beneficial cardiac effect of the pharmacological mechanism (preconditioning and postconditioning) when employed before and after ischemia in patients with ischemic heart disease. Anesthetic preconditioning is related to the dose-dependent signal, while the degree of protection is related to the concentration of the administered drug and the duration of the administration itself. Triggers for postconditioning and preconditioning might have numerous pathways in common; mitochondrial protection and a decrease in inflammatory mediators could be the major biochemical elements...
2017: Drug Design, Development and Therapy
https://www.readbyqxmd.com/read/28345618/ptpip51-regulates-mouse-cardiac-ischemia-reperfusion-through-mediating-the-mitochondria-sr-junction
#8
Xue Qiao, Shi Jia, Jingjing Ye, Xuan Fang, Chenglin Zhang, Yangpo Cao, Chunling Xu, Lifang Zhao, Yi Zhu, Lu Wang, Ming Zheng
Protein tyrosine phosphatase interacting protein 51 (PTPIP51) participates in multiple cellular processes, and dysfunction of PTPIP51 is implicated in diseases such as cancer and neurodegenerative disorders. However, there is no functional evidence showing the physiological or pathological roles of PTPIP51 in the heart. We have therefore investigated the role and mechanisms of PTPIP51 in regulating cardiac function. We found that PTPIP51 was markedly upregulated in ischemia/reperfusion heart. Upregulation of PTPIP51 by adenovirus-mediated overexpression markedly increased the contact of mitochondria-sarcoplasmic reticulum (SR), elevated mitochondrial Ca(2+) uptake from SR release through mitochondrial Ca(2+)uniporter...
March 27, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28342809/identity-and-function-of-a-cardiac-mitochondrial-small-conductance-ca-2-activated-k-channel-splice-variant
#9
MeiYing Yang, Amadou K S Camara, Mohammed Aldakkak, Wai-Meng Kwok, David F Stowe
We provide evidence for location and function of a small conductance, Ca(2+)-activated K(+) (SKCa) channel isoform 3 (SK3) in mitochondria (m) of guinea pig, rat and human ventricular myocytes. SKCa agonists protected isolated hearts and mitochondria against ischemia/reperfusion (IR) injury; SKCa antagonists worsened IR injury. Intravenous infusion of a SKCa channel agonist/antagonist, respectively, in intact rats was effective in reducing/enhancing regional infarct size induced by coronary artery occlusion...
March 22, 2017: Biochimica et Biophysica Acta
https://www.readbyqxmd.com/read/28342806/molecular-regulation-of-mitochondrial-dynamics-in-cardiac-disease
#10
REVIEW
Jinliang Nan, Wei Zhu, M S Rahman, Mingfei Liu, Dan Li, Shengan Su, Na Zhang, Xinyang Hu, Hong Yu, Mahesh P Gupta, Jian''an Wang
Mitochondrial homeostasis is critical for keeping functional heart in response to metabolic or environmental stresses. Mitochondrial fission and fusion (mitochondrial dynamics) play essential roles in maintaining mitochondrial homeostasis, defects in mitochondrial dynamics lead to cardiac diseases such as ischemia-reperfusion injury (IRI), heart failure and diabetic cardiomyopathy. Mitochondrial dynamics is determined by mitochondrial fission and fusion proteins, including OPA1, mitofusins and Drp1. These proteins are tightly regulated by a series of signaling pathways through different aspects such as transcription, post translation modifications (PTMs) and proteasome-dependent protein degradation...
March 22, 2017: Biochimica et Biophysica Acta
https://www.readbyqxmd.com/read/28331061/an-intracellular-matrix-metalloproteinase-2-isoform-induces-tubular-regulated-necrosis-implications-for-acute-kidney-injury
#11
Carla S Ceron, Celine Baligand, Sunil K Joshi, Shaynah Wanga, Patrick M Cowley, Joy P Walker, Sang Heon Song, Rajeev Mahimkar, Anthony J Baker, Robert L Raffai, Zhen J Wang, David H Lovett
Acute kidney injury (AKI) causes severe morbidity, mortality, and chronic kidney disease (CKD). Mortality is particularly marked in the elderly and with pre-existing CKD. Oxidative stress is a common theme in models of AKI induced by ischemia/reperfusion (I/R) injury. We recently characterized an intracellular isoform of matrix metalloproteinase-2 (MMP-2) induced by oxidative stress-mediated activation of an alternate promoter in the first intron of the MMP-2 gene. This generates an N-terminal truncated MMP-2 isoform (NTT-MMP-2) that is intracellular and associated with mitochondria...
March 22, 2017: American Journal of Physiology. Renal Physiology
https://www.readbyqxmd.com/read/28323531/mitophagy-receptor-fundc1-regulates-mitochondrial-homeostasis-and-protects-the-heart-from-i-r-injury
#12
Weilin Zhang, Sami Siraj, Rong Zhang, Quan Chen
Mitophagy plays pivotal roles in the selective disposal of unwanted mitochondria, and accumulation of damaged mitochondria has been linked to aging-related diseases. However, definitive proof that mitophagy regulates mitochondrial quality in vivo is lacking. It is also largely unclear whether damaged mitochondria are the cause or just the consequence of these diseases. We previously showed that FUNDC1 is a mitophagy receptor that interacts with LC3 to mediate mitophagy in response to hypoxia in cultured cells...
March 21, 2017: Autophagy
https://www.readbyqxmd.com/read/28292971/selective-replacement-of-mitochondrial-dna-increases-the-cardioprotective-effect-of-chronic-continuous-hypoxia-in-spontaneously-hypertensive-rats
#13
Jan Neckář, Anna Svatoňová, Romana Weissová, Zdeněk Drahota, Pavlína Zajíčková, Iveta Brabcová, David Kolář, Petra Alánová, Jana Vašinová, Jan Šilhavý, Markéta Hlaváčková, Kateřina Tauchmannová, Marie Milerová, Bohuslav Ošťádal, Luděk Červenka, Jitka Žurmanová, Martin Kalous, Olga Nováková, Jiří Novotný, Michal Pravenec, František Kolář
Mitochondria play an essential role in improved cardiac ischaemic tolerance conferred by adaptation to chronic hypoxia. In the present study, we analysed the effects of continuous normobaric hypoxia (CNH) on mitochondrial functions, including the sensitivity of the mitochondrial permeability transition pore (MPTP) to opening, and infarct size (IS) in hearts of spontaneously hypertensive rats (SHR) and the conplastic SHR-mt(BN) strain, characterized by the selective replacement of the mitochondrial genome of SHR with that of the more ischaemia-resistant brown Norway (BN) strain...
May 1, 2017: Clinical Science (1979-)
https://www.readbyqxmd.com/read/28290047/adaptation-to-chronic-continuous-hypoxia-potentiates-akt-hk2-anti-apoptotic-pathway-during-brief-myocardial-ischemia-reperfusion-insult
#14
David Kolar, Milada Gresikova, Petra Waskova-Arnostova, Barbara Elsnicova, Jana Kohutova, Daniela Hornikova, Pavel Vebr, Jan Neckar, Tereza Blahova, Dita Kasparova, Jiri Novotny, Frantisek Kolar, Olga Novakova, Jitka M Zurmanova
Adaptation to chronic hypoxia represents a potential cardioprotective intervention reducing the extent of acute ischemia/reperfusion (I/R) injury, which is a major cause of death worldwide. The main objective of this study was to investigate the anti-apoptotic Akt/hexokinase 2 (HK2) pathway in hypoxic hearts subjected to I/R insult. Hearts isolated from male Wistar rats exposed either to continuous normobaric hypoxia (CNH; 10% O2) or to room air for 3 weeks were perfused according to Langendorff and subjected to 10 min of no-flow ischemia and 10 min of reperfusion...
March 13, 2017: Molecular and Cellular Biochemistry
https://www.readbyqxmd.com/read/28289383/the-citrus-flavanone-naringenin-produces-cardioprotective-effects-in-hearts-from-1-year-old-rat-through-activation-of-mitobk-channels
#15
Lara Testai, Eleonora Da Pozzo, Ilaria Piano, Luisa Pistelli, Claudia Gargini, Maria Cristina Breschi, Alessandra Braca, Claudia Martini, Alma Martelli, Vincenzo Calderone
Background and Purpose: Incidence of cardiovascular disorders increases with age, because of a dramatic fall of endogenous self-defense mechanisms and increased vulnerability of myocardium. Conversely, the effectiveness of many cardioprotective drugs is blunted in hearts of 1 year old rat. The Citrus flavanone naringenin (NAR) was reported to promote cardioprotective effects against ischemia/reperfusion (I/R) injury, through the activation of mitochondrial large conductance calcium-activated potassium channel (mitoBK)...
2017: Frontiers in Pharmacology
https://www.readbyqxmd.com/read/28274939/long-term-hif-1%C3%AE-transcriptional-activation-is-essential-for-heat-acclimation-mediated-cross-tolerance-mitochondrial-target-genes
#16
Rivka Alexander-Shani, Ahmad Mreisat, Elia Smeir, Gary Gerstenblith, Michael D Stern, Michal Horowitz
An important adaptive feature of heat acclimation (AC) is the induction of cross-tolerance against novel stressors (HACT). Reprogramming of gene expression leading to enhanced innate cytoprotective features by attenuating damage and/or enhancing the response of "help" signals, plays a pivotal role. HIF-1α, constitutively upregulated by AC (1mo, 34°C), is a crucial transcription factor in this program, although its specific role is as yet unknown. By using a rat AC model we studied the impact of disrupting HIF-1α transcriptional activation [(HIF-1α:HIF-1β dimerization blockade by Acriflavine (4mg/kg b...
March 8, 2017: American Journal of Physiology. Regulatory, Integrative and Comparative Physiology
https://www.readbyqxmd.com/read/28272306/akt2-blocks-nucleus-translocation-of-apoptosis-inducing-factor-aif-and-endonuclease-g-endog-while-promoting-caspase-activation-during-cardiac-ischemia
#17
Shuai Yang, Xinmei Zhao, Hui Xu, Fan Chen, Yitao Xu, Zhe Li, Daniel Sanchis, Liang Jin, Yubin Zhang, Junmei Ye
The AKT (protein kinase B, PKB) family has been shown to participate in diverse cellular processes, including apoptosis. Previous studies demonstrated that protein kinase B2 (AKT2(-/-)) mice heart was sensitized to apoptosis in response to ischemic injury. However, little is known about the mechanism and apoptotic signaling pathway. Here, we show that AKT2 inhibition does not affect the development of cardiomyocytes but increases cell death during cardiomyocyte ischemia. Caspase-dependent apoptosis of both the extrinsic and intrinsic pathway was inactivated in cardiomyocytes with AKT2 inhibition during ischemia, while significant mitochondrial disruption was observed as well as intracytosolic translocation of cytochrome C (Cyto C) together with apoptosis-inducing factor (AIF) and endonuclease G (EndoG), both of which are proven to conduct DNA degradation in a range of cell death stimuli...
March 6, 2017: International Journal of Molecular Sciences
https://www.readbyqxmd.com/read/28261301/cardiomyocyte-mitochondria-as-targets-of-humoral-factors-released-by-remote-ischemic-preconditioning
#18
Nilguen Gedik, Leonardo Maciel, Christiane Schulte, Andreas Skyschally, Gerd Heusch, Petra Kleinbongard
INTRODUCTION: Remote ischemic preconditioning (RIPC) reduces myocardial infarct size, and protection can be transferred with plasma to other individuals, even across species. Mitochondria are the end-effectors of cardioprotection by local ischemic conditioning maneuvers. We have now analyzed mitochondrial function in response to RIPC. MATERIAL AND METHODS: Plasma from pigs undergoing placebo or RIPC (infarct size reduction by 67% in RIPC pigs compared to placebo) was transferred to isolated perfused rat hearts subjected to 30 min global ischemia followed by 120 min reperfusion for infarct size measurement...
March 1, 2017: Archives of Medical Science: AMS
https://www.readbyqxmd.com/read/28258543/reducing-mitochondrial-bound-hexokinase-ii-mediates-transition-from-non-injurious-into-injurious-ischemia-reperfusion-of-the-intact-heart
#19
Rianne Nederlof, Ebru Gürel-Gurevin, Otto Eerbeek, Chaoqin Xie, G Sjoerd Deijs, Moritz Konkel, Jun Hu, Nina C Weber, Cees A Schumacher, Antonius Baartscheer, Egbert G Mik, Markus W Hollmann, Fadi G Akar, Coert J Zuurbier
Ischemia/reperfusion (I/R) of the heart becomes injurious when duration of the ischemic insult exceeds a certain threshold (approximately ≥20 min). Mitochondrial bound hexokinase II (mtHKII) protects against I/R injury, with the amount of mtHKII correlating with injury. Here, we examine whether mtHKII can induce the transition from non-injurious to injurious I/R, by detaching HKII from mitochondria during a non-injurious I/R interval. Additionally, we examine possible underlying mechanisms (increased reactive oxygen species (ROS), increased oxygen consumption (MVO2) and decreased cardiac energetics) associated with this transition...
March 3, 2017: Journal of Physiology and Biochemistry
https://www.readbyqxmd.com/read/28249782/aldh2-restores-exhaustive-exercise-induced-mitochondrial-dysfunction-in-skeletal-muscle
#20
Qiuping Zhang, Jianheng Zheng, Jun Qiu, Xiahong Wu, Yangshuo Xu, Weili Shen, Mengwei Sun
BACKGROUND: Mitochondrial aldehyde dehydrogenase 2 (ALDH2) is highly expressed in heart and skeletal muscles, and is the major enzyme that metabolizes acetaldehyde and toxic aldehydes. The cardioprotective effects of ALDH2 during cardiac ischemia/reperfusion injury have been recognized. However, less is known about the function of ALDH2 in skeletal muscle. This study was designed to evaluate the effect of ALDH2 on exhaustive exercise-induced skeletal muscle injury. METHODS: We created transgenic mice expressing ALDH2 in skeletal muscles...
April 15, 2017: Biochemical and Biophysical Research Communications
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