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heart and ischemia and mitochondria

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https://www.readbyqxmd.com/read/28802666/humanin-directly-protects-cardiac-mitochondria-against-dysfunction-initiated-by-oxidative-stress-by-decreasing-complex-i-activity
#1
Savitree Thummasorn, Krekwit Shinlapawittayatorn, Juthamas Khamseekaew, Thidarat Jaiwongkam, Siriporn C Chattipakorn, Nipon Chattipakorn
Humanin (HN) is an endogenous peptide that exerts cytoprotection against oxidative stress and apoptosis. We recently reported that Humanin analogue (HNG) pretreatment can reduce reactive oxygen species production in the heart subjected to ischemia/reperfusion (I/R) injury via attenuating mitochondrial dysfunction. However, it is unclear if HNG has direct effects on mitochondrial function against oxidative stress. Thus, we sought to determine the effects of HNG on mitochondrial function under hydrogen peroxide (H2O2) induced oxidative stress in isolated cardiac mitochondria...
August 9, 2017: Mitochondrion
https://www.readbyqxmd.com/read/28795196/melatonin-and-mitochondrial-function-during-ischemia-reperfusion-injury
#2
REVIEW
Zhiqiang Ma, Zhenlong Xin, Wencheng Di, Xiaolong Yan, Xiaofei Li, Russel J Reiter, Yang Yang
Ischemia/reperfusion (IR) injury occurs in many organs and tissues, and contributes to morbidity and mortality worldwide. Melatonin, an endogenously produced indolamine, provides a strong defense against IR injury. Mitochondrion, an organelle for ATP production and a decider for cell fate, has been validated to be a crucial target for melatonin to exert its protection against IR injury. In this review, we first clarify the mechanisms underlying mitochondrial dysfunction during IR and melatonin's protection of mitochondria under this condition...
August 9, 2017: Cellular and Molecular Life Sciences: CMLS
https://www.readbyqxmd.com/read/28777255/endogenous-and-agonist-induced-opening-of-mitochondrial-big-vs-small-ca2-sensitive-k-channels-on-cardiac-cell-and-mitochondrial-protection
#3
David F Stowe, Meiying Yang, James S Heisner, Amadou K S Camara
Both big (BKCa) and small (SKCa) conductance Ca-sensitive K channels are present in mammalian cardiac cell mitochondria (m). We used pharmacological agonists and antagonists of BKCa and SKCa channels to examine the importance of endogenous opening of these channels and the relative contribution of either or both of these channels to protect against contractile dysfunction and reduce infarct size after ischemia reperfusion (IR) injury through a mitochondrial protective mechanism. Following global cardiac IR injury of ex vivo perfused guinea pig hearts we found the following: both agonists NS1619 (for BKCa) and DCEB (for SKCa) improved contractility; BKCa antagonist paxilline (PAX) alone or with SKCa antagonist NS8593 worsened contractility and enhanced infarct size; both antagonists PAX and NS8593 obliterated protection by their respective agonists; BKCa and SKCa antagonists did not block protection afforded by SKCa and BKCa agonists, respectively; and all protective effects by the agonists were blocked by scavenging superoxide anions (O2) with TBAP...
August 4, 2017: Journal of Cardiovascular Pharmacology
https://www.readbyqxmd.com/read/28776263/age-and-ischemia-differentially-impact-mitochondrial-ultrastructure-and-function-in-a-novel-model-of-age-associated-estrogen-deficiency-in-the-female-rat-heart
#4
Alexandra M Garvin, Nicole C Aurigemma, Jenna L Hackenberger, Donna H Korzick
Altered mitochondrial respiration, morphology, and quality control collectively contribute to mitochondrial dysfunction in the aged heart. Because myocardial infarction remains the leading cause of death in aged women, the present study utilized a novel rodent model to recapitulate human menopause to interrogate the combination of age and estrogen deficiency on mitochondrial ultrastructure and function with cardiac ischemia/reperfusion (I/R) injury. Female F344 rats were ovariectomized (OVX) at 15 months and studied at 24 months (MO OVX; n = 40) vs adult ovary intact (6 months; n = 41)...
August 4, 2017: Pflügers Archiv: European Journal of Physiology
https://www.readbyqxmd.com/read/28736742/unique-morphological-characteristics-of-mitochondrial-subtypes-in-the-heart-the-effect-of-ischemia-and-ischemic-preconditioning
#5
Siavash Beikoghli Kalkhoran, Peter Munro, Fan Qiao, Sang-Bing Ong, Andrew R Hall, Hector Cabrera-Fuentes, Bibhas Chakraborty, William A Boisvert, Derek M Yellon, Derek J Hausenloy
RATIONALE: Three subsets of mitochondria have been described in adult cardiomyocytes - intermyofibrillar (IMF), subsarcolemmal (SSM), and perinuclear (PN). They have been shown to differ in physiology, but whether they also vary in morphological characteristics is unknown. Ischemic preconditioning (IPC) is known to prevent mitochondrial dysfunction induced by acute myocardial ischemia/reperfusion injury (IRI), but whether IPC can also modulate mitochondrial morphology is not known. AIMS: Morphological characteristics of three different subsets of adult cardiac mitochondria along with the effect of ischemia and IPC on mitochondrial morphology will be investigated...
January 2017: Discoveries
https://www.readbyqxmd.com/read/28736181/succinate-accumulation-impairs-cardiac-pyruvate-dehydrogenase-activity-through-grp91-dependent-and-independent-signaling-pathways-therapeutic-effects-of-ginsenoside-rb1
#6
Jia Li, Yi-Lin Yang, Lan-Zhu Li, Lei Zhang, Qun Liu, Kang Liu, Ping Li, Baolin Liu, Lian-Wen Qi
Altered mitochondrial oxidation increases vulnerability to cardiac ischemia/reperfusion (I/R) injury in metabolic disorders. However, the metabolic signaling responsible for the dysfunction remains partly unknown. We sought to test whether or not hypoxic succinate accumulation could inhibit pyruvate dehydrogenase (PDH) activity and subsequently aggravate I/R injury. Results showed that saturated fatty acid palmitate stimulation increased fatty acid oxidation and induced hypoxia in cardiomyocytes, leading to succinate accumulation...
July 20, 2017: Biochimica et Biophysica Acta
https://www.readbyqxmd.com/read/28730272/mitochondria-as-a-target-of-cardioprotection-in-models-of-preconditioning
#7
REVIEW
Magdaléna Jašová, Ivana Kancirová, Iveta Waczulíková, Miroslav Ferko
Over the recent years the view on mitochondria in the heart as a cellular powerhouse providing ATP supply needed to sustain contractile function, basal metabolic processes, and ionic homeostasis has changed radically. At present it is known that dysfunctions of these organelles are essential in the development of a large number of diseases, including cardiovascular diseases. Moreover, mitochondria are considered to be a very promising target of endogenous strategies that are essential in the protection of the myocardium from acute ischemia/reperfusion injury...
July 20, 2017: Journal of Bioenergetics and Biomembranes
https://www.readbyqxmd.com/read/28712398/-fasudil-attenuates-mitochondrial-injury-and-apoptosis-in-rat-model-of-myocardial-ischemia-reperfusion-injury
#8
Hongwei Ye, Guanjun Zhang, Ruiping Cao, Pinfang Kang, Zhenghong Li, Qin Gao
Objective To observe the changes of mitochondria fusion protein 2 (Mfn2) and dynamin-related protein 1 (Drp1) in the cardioprotection of fasudil, and analyze the significance. Methods Hearts isolated from male Sprague-Dawley rats were subjected to ischemia for 30 minutes (occlusion of left anterior descending artery), and continuously perfusion for 120 minutes to establish myocardial ischemia/reperfusion (I/R) injury model. The rats were divided into 3 groups: sham group, I/R group and fasudil group. The left ventricular hemodynamics were continuously recorded; lactate dehydrogenase (LDH) content was measured during reperfusion; myocardial ultrastructure was observed by electron microscopy; the protein expression of phosphorylated protein phosphatase 1 regulatory subunit 12A (p-PPP1R12A/p-MYPT1) was detected by immunohistochemistry; and the protein expressions of Mfn2, Drp1 and cleaved caspase-3 (c-caspase-3) were detected by Western blot analysis...
July 2017: Xi Bao Yu Fen Zi Mian Yi Xue za Zhi, Chinese Journal of Cellular and Molecular Immunology
https://www.readbyqxmd.com/read/28689004/the-role-of-succinate-and-ros-in-reperfusion-injury-a-critical-appraisal
#9
REVIEW
Tatyana N Andrienko, Philippe Pasdois, Gonçalo C Pereira, Matthew J Ovens, Andrew P Halestrap
We critically assess the proposal that succinate-fuelled reverse electron flow (REF) drives mitochondrial matrix superoxide production from Complex I early in reperfusion, thus acting as a key mediator of ischemia/reperfusion (IR) injury. Real-time surface fluorescence measurements of NAD(P)H and flavoprotein redox state suggest that conditions are unfavourable for REF during early reperfusion. Furthermore, rapid loss of succinate accumulated during ischemia can be explained by its efflux rather than oxidation...
July 5, 2017: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/28685325/potential-signaling-pathways-of-acute-endurance-exercise-induced-cardiac-autophagy-and-mitophagy-and-its-possible-role-in-cardioprotection
#10
REVIEW
Youngil Lee, Insu Kwon, Yongchul Jang, Wankeun Song, Ludmila M Cosio-Lima, Mark H Roltsch
Cardiac myocytes are terminally differentiated cells and possess extremely limited regenerative capacity; therefore, preservation of mature cardiac myocytes throughout the individual's entire life span contributes substantially to healthy living. Autophagy, a lysosome-dependent cellular catabolic process, is essential for normal cardiac function and mitochondria maintenance. Therefore, it may be reasonable to hypothesize that if endurance exercise promotes cardiac autophagy and mitochondrial autophagy or mitophagy, exercise-induced cardiac autophagy (EICA) or exercise-induced cardiac mitophagy (EICM) may confer propitious cellular environment and thus protect the heart against detrimental stresses, such as an ischemia-reperfusion (I/R) injury...
July 6, 2017: Journal of Physiological Sciences: JPS
https://www.readbyqxmd.com/read/28642067/caloric-restriction-protects-livers-from-ischemia-reperfusion-damage-by-preventing-ca-2-induced-mitochondrial-permeability-transition
#11
Sergio L Menezes-Filho, Ignacio Amigo, Fernanda M Prado, Natalie C Ferreira, Marcia K Koike, Isabella F D Pinto, Sayuri Miyamoto, Edna F S Montero, Marisa H G Medeiros, Alicia J Kowaltowski
Caloric restriction (CR) promotes lifespan extension and protects against many pathological conditions, including ischemia/reperfusion injury to the brain, heart and kidney. In the liver, ischemia/reperfusion damage is related to excessive mitochondrial Ca(2+) accumulation, leading to the mitochondrial permeability transition. Indeed, liver mitochondria isolated from animals maintained on CR for 4 months were protected against permeability transition and capable of taking up Ca(2+) at faster rates and in larger quantities...
June 19, 2017: Free Radical Biology & Medicine
https://www.readbyqxmd.com/read/28641785/acute-detachment-of-hexokinase-ii-from-mitochondria-modestly-increases-oxygen-consumption-of-the-intact-mouse-heart
#12
Rianne Nederlof, Simone Denis, Benjamin Lauzier, Christine Des Rosiers, Markku Laakso, Jacob Hagen, Carmen Argmann, Ronald Wanders, Riekelt H Houtkooper, Markus W Hollmann, Sander M Houten, Coert J Zuurbier
OBJECTIVE: Cardiac hexokinase II (HKII) can translocate between cytosol and mitochondria and change its cellular expression with pathologies such as ischemia-reperfusion, diabetes and heart failure. The cardiac metabolic consequences of these changes are unknown. Here we measured energy substrate utilization in cytosol and mitochondria using stabile isotopes and oxygen consumption of the intact perfused heart for 1) an acute decrease in mitochondrial HKII (mtHKII), and 2) a chronic decrease in total cellular HKII...
July 2017: Metabolism: Clinical and Experimental
https://www.readbyqxmd.com/read/28641075/postconditioning-with-intralipid-emulsion-protects-against-reperfusion-injury-in-post-infarct-remodeled-rat-hearts-by-activation-of-ros-akt-erk-signaling
#13
Michael Zaugg, Phing-How Lou, Eliana Lucchinetti, Manoj Gandhi, Alexander S Clanachan
The clinically used lipid emulsion Intralipid (ILE) reduces ischemia reperfusion injury in healthy rodent hearts. We tested whether ILE is cardioprotective in postinfarct remodeled hearts. Post-infarct remodeled and sham Sprague-Dawley rat hearts were perfused in working mode and subjected to ischemia (15 minutes) and reperfusion (30 minutes). Left ventricular (LV) work was measured in hearts that were untreated or that received ILE (1%) postconditioning administered at the onset of reperfusion, or the reactive oxygen species (ROS) scavenger N-(2-mercaptopropionyl)-glycine (10 μM) alone or in combination with ILE...
June 1, 2017: Translational Research: the Journal of Laboratory and Clinical Medicine
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
#14
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
#15
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
#16
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
#17
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
#18
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
#19
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
#20
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
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