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heart and ischemia and mitochondria

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https://www.readbyqxmd.com/read/28619102/dl-3-n-butylphthalide-protects-the-heart-against-ischemic-injury-and-h9c2-cardiomyoblasts-against-oxidative-stress-involvement-of-mitochondrial-function-and-biogenesis
#1
Xiaochao Tian, Weiliang He, Rong Yang, Yingping Liu
BACKGROUND: Myocardial infarction (MI) is an acute and fatal condition that threatens human health. Dl-3-n-butylphthalide (NBP) has been used for the treatment of acute ischemic stroke. Mitochondria may play a protective role in MI injury. However, there are few reports on the cardioprotective effect of NBP or the potential mitochondrial mechanism for the NBP-induced protection against cardiac ischemia injury. We investigated the therapeutic effects of NBP in an in vivo MI model and an in vitro oxidative stress model, as well as the potential mitochondrial mechanism...
June 15, 2017: Journal of Biomedical Science
https://www.readbyqxmd.com/read/28598489/nicotinic-acetylcholine-receptor-mediated-protection-of-the-rat-heart-exposed-to-ischemia-reperfusion
#2
Spyros A Mavropoulos, Nayaab S Khan, Asaph C J Levy, Bradley T Faliks, Cristina P Sison, Valentin A Pavlov, Youhua Zhang, Kaie Ojamaa
Reperfusion injury following acute myocardial infarction is associated with significant morbidity. Activation of neuronal or non-neuronal cholinergic pathways in the heart has been shown to reduce ischemic injury and this effect has been attributed primarily to muscarinic acetylcholine receptors. In contrast, the role of nicotinic receptors, specifically alpha-7 subtype (α7nAChR) in the myocardium remains unknown which offers an opportunity to potentially repurpose several agonists/modulators that are currently under development for neurologic indications...
June 8, 2017: Molecular Medicine
https://www.readbyqxmd.com/read/28595547/beneficial-effects-of-n-acetylcysteine-and-n-mercaptopropionylglycine-on-ischemia-reperfusion-injury-in-the-heart
#3
Monika Bartekova, Miroslav Barancik, Kristina Ferenczyova, Narajan S Dhalla
Ischemia-reperfusion (I/R) injury of the heart as a consequence of myocardial infarction or cardiac surgery represents a serious clinical problem. One of the most prominent mechanisms of I/R injury is the development of oxidative stress in the heart. In this regard, I/R has been shown to enhance the production of reactive oxygen/nitrogen species in the heart which lead to the imbalance between the pro-oxidants and antioxidant capacities of the endogenous radical-scavenging systems. Accordingly, increasing the antioxidant capacity of the heart by the administration of exogenous antioxidants is considered beneficial for the heart exposed to I/R...
June 8, 2017: Current Medicinal Chemistry
https://www.readbyqxmd.com/read/28579963/olesoxime-inhibits-cardioplegia-induced-ischemia-reperfusion-injury-a-study-in-langendorff-perfused-rabbit-hearts
#4
Aida Salameh, Maren Keller, Ingo Dähnert, Stefan Dhein
Objective: During cardioplegia, which is often used in cardiac surgery, the heart is subjected to global ischemia/reperfusion injury, which can result in a post-operative impairment of cardiac function. Mitochondria permeability transition pores (MPTP) play a key role in cardiomyocyte survival after ischemia/reperfusion injury. It was shown in clinical settings that blockers of MPTP like cyclosporine might have a positive influence on cardiac function after cardioplegic arrest. Olesoxime, which is a new drug with MPTP blocking activity, has been introduced as a neuroprotective therapeutic agent...
2017: Frontiers in Physiology
https://www.readbyqxmd.com/read/28560002/prostaglandin-e1-protects-coronary-microvascular-function-via-the-glycogen-synthase-kinase-3%C3%AE-mitochondrial-permeability-transition-pore-pathway-in-rat-hearts-subjected-to-sodium-laurate-induced-coronary-microembolization
#5
Houyong Zhu, Yu Ding, Xiaoqun Xu, Meiya Li, Yangliang Fang, Beibei Gao, Hengyi Mao, Guoxin Tong, Liang Zhou, Jinyu Huang
Prostaglandin E1 (PGE1) is used as a pretreatment for ischemia reperfusion injury in many biological systems. However, its value as a pretreatment for coronary microembolization (CME) is unknown. The goal of this study was to determine whether PGE1 would protect against CME. In a CME rat model, we observed microthrombi and early myocardial ischemia, with endothelium appearing exfoliated and mitochondria having irregular morphology and decreased internal complexity. The level of fibrinogen-like protein 2 prothrombinase was increased and superoxide dismutase and catalase levels were decreased...
2017: American Journal of Translational Research
https://www.readbyqxmd.com/read/28559847/high-sensitivity-of-sirt3-deficient-hearts-to-ischemia-reperfusion-is-associated-with-mitochondrial-abnormalities
#6
Rebecca M Parodi-Rullán, Xavier Chapa-Dubocq, Pedro J Rullán, Sehwan Jang, Sabzali Javadov
Aim: Sirtuins are NAD(+)-dependent deacetylases that regulate cell metabolism through protein acetylation/deacetylation, and SIRT3 is the major deacetylase among mitochondrial isoforms. Here, we elucidated the possible role of acetylation of cyclophilin D, a key regulator of the mitochondrial permeability transition pore (mPTP), in mitochondria-mediated cardiac dysfunction induced by ischemia-reperfusion (IR) in wild type (WT) and SIRT3 knockout (SIRT3(-/-)) mice. Materials and Methods: Isolated and Langendorff-mode perfused hearts of WT and SIRT3(-/-) mice were subjected to 25-min global ischemia followed by 60-min of reperfusion in the presence or absence of the mPTP inhibitor, sanglifehrin A (SfA)...
2017: Frontiers in Pharmacology
https://www.readbyqxmd.com/read/28554327/vdac-targeted-drugs-affecting-cytoprotection-and-mitochondrial-physiology-in-cerebrovascular-and-cardiovascular-diseases
#7
Andonis Karachitos, Joaquin Jordan, Hanna Kmita
Cerebrovascular and cardiovascular diseases are caused by impairment of the brain and/or heart circulation. Insufficient blood flow results in a decrease in oxygen delivery (ischemia) which affects mitochondria functioning and consequently lead to insufficient ATP production. Moreover, ischemia combined with the following reperfusion may result in further mitochondria dysfunction coexisting with lower ATP synthesis and higher ROS generation This, in turn, have direct implications in the pathogenesis of cerebrovascular and cardiovascular diseases...
May 29, 2017: Current Medicinal Chemistry
https://www.readbyqxmd.com/read/28551809/mitochondrial-transplantation-in-myocardial-ischemia-and-reperfusion-injury
#8
Borami Shin, Douglas B Cowan, Sitaram M Emani, Pedro J Del Nido, James D McCully
Ischemic heart disease remains the leading cause of death worldwide. Mitochondria are the power plant of the cardiomyocyte, generating more than 95% of the cardiac ATP. Complex cellular responses to myocardial ischemia converge on mitochondrial malfunction which persists and increases after reperfusion, determining the extent of cellular viability and post-ischemic functional recovery. In a quest to ameliorate various points in pathways from mitochondrial damage to myocardial necrosis, exhaustive pharmacologic and genetic tools have targeted various mediators of ischemia and reperfusion injury and procedural techniques without applicable success...
2017: Advances in Experimental Medicine and Biology
https://www.readbyqxmd.com/read/28551796/nitrite-nitric-oxide-signaling-and-cardioprotection
#9
Matthias Totzeck, Ulrike B Hendgen-Cotta, Tienush Rassaf
Cardioprotective strategies to prevent damage to mitochondria in acute myocardial infarction are warranted to reduce lethal myocardial ischemia/reperfusion (I/R) injury. Mitochondrial antagonists in I/R are reactive oxygen species (ROS), deteriorated calcium signaling, permeabilization of the mitochondrial outer membrane (MOM) and deranged mitochondrial structural dynamism (fusion and fission). Nitric oxide (NO) related signaling can protect hearts from I/R. Albeit the underlying signaling is incompletely resolved, recent data point to a particular involvement of protective posttranslational modification of mitochondrial elements...
2017: Advances in Experimental Medicine and Biology
https://www.readbyqxmd.com/read/28551793/mitochondria-in-structural-and-functional-cardiac-remodeling
#10
Natalia Torrealba, Pablo Aranguiz, Camila Alonso, Beverly A Rothermel, Sergio Lavandero
The heart must function continuously as it is responsible for both supplying oxygen and nutrients throughout the entire body, as well as for the transport of waste products to excretory organs. When facing either a physiological or pathological increase in cardiac demand, the heart undergoes structural and functional remodeling as a means of adapting to increased workload. These adaptive responses can include changes in gene expression, protein composition, and structure of sub-cellular organelles involved in energy production and metabolism...
2017: Advances in Experimental Medicine and Biology
https://www.readbyqxmd.com/read/28551790/connexin-43-and-mitochondria-in-cardiovascular-health-and-disease
#11
Kerstin Boengler, Rainer Schulz
Connexin 43 (Cx43) is the major connexin protein in ventricular cardiomyocytes. Six Cx43 proteins assemble into so-called hemichannels at the sarcolemma and opposing hemichannels form gap junctions, which allow the passage of small molecules and electrical current flow between adjacent cells. Apart from its localization at the plasma membrane, Cx43 is also present in cardiomyocyte mitochondria, where it is important for mitochondrial function in terms of oxygen consumption and potassium fluxes. The expression of gap junctional and mitochondrial Cx43 is altered under several pathophysiological conditions among them are hypertension, hypertrophy, hypercholesterolemia, ischemia/reperfusion injury, post-infarction remodeling, and heart failure...
2017: Advances in Experimental Medicine and Biology
https://www.readbyqxmd.com/read/28551786/mitochondrial-bioenergetics-during-ischemia-and-reperfusion
#12
Alicia E Consolini, María I Ragone, Patricia Bonazzola, Germán A Colareda
During ischemia and reperfusion (I/R) mitochondria suffer a deficiency to supply the cardiomyocyte with chemical energy, but also contribute to the cytosolic ionic alterations especially of Ca(2+). Their free calcium concentration ([Ca(2+)]m) mainly depends on mitochondrial entrance through the uniporter (UCam) and extrusion in exchange with Na(+) (mNCX) driven by the electrochemical gradient (ΔΨm). Cardiac energetic is frequently estimated by the oxygen consumption, which determines metabolism coupled to ATP production and to the maintaining of ΔΨm...
2017: Advances in Experimental Medicine and Biology
https://www.readbyqxmd.com/read/28551785/mitochondria-in-ischemic-heart-disease
#13
L Maximilian Buja
A core feature of ischemic heart disease is injury to cardiomyocytes (CMC). Ischemic CMC manifest the molecular mechanisms to undergo the major forms of cell injury and death, namely, oncotic necrosis, necroptosis, apoptosis and unregulated autophagy. Important modulators of ischemic injury are reperfusion and conditioning. Mitochondria have a major role in mediating the injury to CMC through membrane protein complexes referred to as death channels. Apoptosis is mediated by activation of a channel regulated by the Bcl-2 protein family leading to mitochondrial outer membrane permeabilization (MOMP)...
2017: Advances in Experimental Medicine and Biology
https://www.readbyqxmd.com/read/28528298/emerging-role-of-monoamine-oxidase-as-a-therapeutic-target-for-cardiovascular-disease
#14
REVIEW
Soni Deshwal, Moises Di Sante, Fabio Di Lisa, Nina Kaludercic
In the past decade, accumulating evidence highlighted the role of monoamine oxidases (MAOs) in cardiovascular disease (CVD). MAOs are flavoenzymes located in the outer mitochondrial membrane, responsible for the degradation of neurotransmitters and biogenic amines. During this process they generate hydrogen peroxide, aldehydes and ammonia, species that can target mitochondria and induce mitochondrial dysfunction and cardiomyocyte death. Indeed, MAO inhibition affords cardioprotection in several models of CVD, such as ischemia/reperfusion, heart failure and diabetes...
May 18, 2017: Current Opinion in Pharmacology
https://www.readbyqxmd.com/read/28524859/mesenchymal-stem-cells-sense-mitochondria-released-from-damaged-cells-as-danger-signals-to-activate-their-rescue-properties
#15
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/28508960/impairment-of-ph-gradient-and-membrane-potential-mediates-redox-dysfunction-in-the-mitochondria-of-the-post-ischemic-heart
#16
Patrick T Kang, Chwen-Lih Chen, Paul Lin, William M Chilian, Yeong-Renn Chen
The mitochondrial electrochemical gradient (Δp), which comprises the pH gradient (ΔpH) and the membrane potential (ΔΨ), is crucial in controlling energy transduction. During myocardial ischemia and reperfusion (IR), mitochondrial dysfunction mediates superoxide ((·)O2(-)) and H2O2 overproduction leading to oxidative injury. However, the role of ΔpH and ΔΨ in post-ischemic injury is not fully established. Here we studied mitochondria from the risk region of rat hearts subjected to 30 min of coronary ligation and 24 h of reperfusion in vivo...
July 2017: Basic Research in Cardiology
https://www.readbyqxmd.com/read/28450394/reactive-oxygen-species-production-induced-by-pore-opening-in-cardiac-mitochondria-the-role-of-complex-ii
#17
Paavo Korge, Scott A John, Guillaume Calmettes, James N Weiss
Succinate-driven reverse electron transport (RET) through complex I is hypothesized to be a major source of reactive oxygen species (ROS) that induces permeability transition pore (PTP) opening and damages the heart during ischemia/reperfusion. Because RET can only generate ROS when mitochondria are fully polarized, this mechanism is self-limiting once PTP opens during reperfusion. In the accompanying article (Korge, P., Calmettes, G., John, S. A., and Weiss, J. N. (2017) J. Biol. Chem. 292, 9882-9895), we showed that ROS production after PTP opening can be sustained when complex III is damaged (simulated by antimycin)...
June 16, 2017: Journal of Biological Chemistry
https://www.readbyqxmd.com/read/28421373/role-of-glycogen-synthase-kinase-following-myocardial-infarction-and-ischemia-reperfusion
#18
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...
July 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
#19
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
#20
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%. 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 15min of CA...
July 2017: Resuscitation
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