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heart and ischemia and mitochondria

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https://www.readbyqxmd.com/read/29130663/-capsaicin-alleviate-myocardial-ischemia-reperfusion-injury-through-attenuating-mitochondrial-oxidative-stress
#1
Juan-Xia Zhu, Ling-Heng Kong, Chao-Feng Zhang, Na Sun, Jin-Rui Chang, Yan Xu
OBJECTIVE: To investigate the role of capsaicin (CAP) in myocardial ischemia reperfusion injury and its underlying mechanisms. METHODS: Twentyfour adult male SD rats were randomized into 4 groups,namely the control group,ischemia reperfusion group,ischemia reperfusion with CAP group,and ischemia reperfusion with CAPZ and CAP group. Isolated rat hearts underwent Langendorff perfusion. Left ventricular enddiastolic pressure (LVEDP) andleft ventricular developed pressure (LVDP) was calculated to evaluate myocardial performance at 30 min of reperfusion...
September 2017: Sichuan da Xue Xue Bao. Yi Xue Ban, Journal of Sichuan University. Medical Science Edition
https://www.readbyqxmd.com/read/29104640/penehyclidine-hydrochloride-post-conditioning-reduces-ischemia-reperfusion-induced-cardiomyocyte-apoptosis-in-rats
#2
Hongbao Tan, Li Chen, Jun Ma
Ischemic heart disease is a major cause of mortality and disability worldwide. Timely reperfusion is currently the most effective method of treating ischemic heart disease; however, abrupt reperfusion may cause ischemia/reperfusion (I/R) injury. Apoptosis serves an important role in the progression of myocardial I/R injury and it has been demonstrated that the mitochondria are the center of regulation for apoptosis. Penehyclidine hydrochloride (PHC) is used during surgery and has recently been identified as a new type of anticholinergic drug...
November 2017: Experimental and Therapeutic Medicine
https://www.readbyqxmd.com/read/29101177/a-novel-mitochondrial-dna-repair-enzyme-attenuates-maladaptive-remodeling-and-preserves-cardiac-function-in-heart-failure
#3
Jessica M Bradley, Zhen Li, Chelsea L Organ, David J Polhemus, Hiroyuki Otsuka, Shashi Bhushan, Olena M Gorodnya, Mykhaylo Ruchko, Mark N Gillespie, Glenn L Wilson, David J Lefer
BACKGROUND: Oxidative stress results in mitochondrial DNA (mtDNA) damage and contributes to myocardial cell death. mtDNA repair enzymes are crucial for mtDNA repair and cell survival. We investigated a novel, mitochondrial-targeted fusion protein (Exscien1-III) containing endonuclease III in myocardial ischemia/reperfusion (MI/Rep) injury and transverse aortic constriction (TAC) induced heart failure. METHODS AND RESULTS: Male C57/BL6J mice (10-12 wks) were subjected to 45 min...
November 3, 2017: American Journal of Physiology. Heart and Circulatory Physiology
https://www.readbyqxmd.com/read/29091875/role-of-endogenous-hydrogen-sulfide-in-cardiac-mitochondrial-preservation-during-ischemia-reperfusion-injury
#4
Sanhitha Nandi, Sriram Ravindran, Gino A Kurian
Cardio-protective effect of hydrogen sulfide (H2S) against myocardial ischemia reperfusion injury (I/R) via preservation of mitochondria is well documented. But the distinct role of exogenous and endogenous H2S in cardio-protection and its dependency on functional cardiac mitochondria is not understood. The present study was designed to investigate the role of exogenous H2S preconditioning on cardiac mitochondrial subpopulation namely interfibrillar (IFM) and subsarcolemmal (SSM), in attenuating I/R injury in an isolated rat heart model in the absence of endogenous H2S production...
October 26, 2017: Biomedicine & Pharmacotherapy, Biomédecine & Pharmacothérapie
https://www.readbyqxmd.com/read/29063106/-recent-progress-of-mitochondrial-quality-control-in-ischemic-heart-disease-and-its-role-in-cardio-protection-of-vagal-nerve
#5
Run-Qing Xue, Man Xu, Xiao-Jiang Yu, Long-Zhu Liu, Wei-Jin Zang
Ischemic heart disease (IHD) is the life-threatening cardiovascular disease. Mitochondria have emerged as key participants and regulators of cellular energy demands and signal transduction. Mitochondrial quality is controlled by a number of coordinated mechanisms including mitochondrial fission, fusion and mitophagy, which plays an important role in maintaining healthy mitochondria and cardiac function. Recently, dysfunction of each process in mitochondrial quality control has been observed in the ischemic hearts...
October 25, 2017: Sheng Li Xue Bao: [Acta Physiologica Sinica]
https://www.readbyqxmd.com/read/29054138/mdivi-1-protects-human-w8b2-cardiac-stem-cells-from-oxidative-stress-and-simulated-ischemia-reperfusion-injury
#6
Ayeshah A Rosdah, Simon T Bond, Priyadharshini Sivakumaran, Ashfaqul Hoque, Jonathan S Oakhill, Brian G Drew, Lea Md Delbridge, Shiang Yong Lim
Cardiac stem cell (CSC) therapy is a promising approach to treat ischemic heart disease. However, the poor survival of transplanted stem cells in the ischemic myocardium has been a major impediment in achieving an effective cell-based therapy against myocardial infarction. Inhibiting mitochondrial fission has been shown to promote survival of several cell types. However, the role of mitochondrial morphology in survival of human CSC remains unknown. In this study, we investigated whether Mdivi-1, an inhibitor of mitochondrial fission protein Drp1, can improve survival of a novel population of human W8B2+ CSCs in hydrogen peroxide-induced oxidative stress and simulated ischemia-reperfusion injury models...
October 20, 2017: Stem Cells and Development
https://www.readbyqxmd.com/read/29051737/lack-of-contribution-of-p66shc-and-its-mitochondrial-translocation-to-ischemia-reperfusion-injury-and-cardioprotection-by-ischemic-preconditioning
#7
Kerstin Boengler, Péter Bencsik, János Palóczi, Krisztina Kiss, Márton Pipicz, Judit Pipis, Péter Ferdinandy, Klaus-Dieter Schlüter, Rainer Schulz
Whereas high amounts of reactive oxygen species (ROS) contribute to cardiac damage following ischemia and reperfusion (IR), low amounts function as trigger molecules in the cardioprotection by ischemic preconditioning (IPC). The mitochondrial translocation and contribution of the hydrogen peroxide-generating protein p66shc in the cardioprotection by IPC is unclear yet. In the present study, we investigated the mitochondrial translocation of p66shc, addressed the impact of p66shc on ROS formation after IR, and characterized the role of p66shc in IR injury per se and in the cardioprotection by IPC...
2017: Frontiers in Physiology
https://www.readbyqxmd.com/read/29040818/metformin-attenuates-er-stress-induced-mitochondrial-dysfunction
#8
Qun Chen, Jeremy Thompson, Ying Hu, Anindita Das, Edward J Lesnefsky
Endoplasmic reticulum (ER) stress, a disturbance of the ER function, contributes to cardiac injury. ER and mitochondria are closely connected organelles within cells. ER stress contributes to mitochondrial dysfunction, which is a key factor to increase cardiac injury. Metformin, a traditional anti-diabetic drug, decreases cardiac injury during ischemia-reperfusion. Metformin also inhibits ER stress in cultured cells. We hypothesized that metformin can attenuate the ER stress-induced mitochondrial dysfunction and subsequent cardiac injury...
September 28, 2017: Translational Research: the Journal of Laboratory and Clinical Medicine
https://www.readbyqxmd.com/read/28899492/tilianin-pretreatment-prevents-myocardial-ischemia-reperfusion-injury-via-preservation-of-mitochondrial-function-in-rat-heart
#9
Yong Yuan, Wenjiang Cao, Ye Hong, Xinhong Guo, Yanfang Wang, Yangyang Wang, Xinchun Wang, Ping Hu
BACKGROUND: Tilianin has been demonstrated to exert protective effects on the heart against ischemia-reperfusion (I/R) injury, yet whether it is beneficial to the mitochondria during myocardial I/R is unclear. METHODS: In this study, we demonstrated that pretreatment with Tilianin dose-dependently raised the levels of ATP of the myocardium, and protected the microstructures and functions of mitochondria in rats. Furthermore, the cytoprotective effect of Tilianin has been confirmed in vivo and in the H9c2 cardiomyoblast cell line with enhancing activities of the mitochondria, controlling the levels of Ca(2+) and reactive oxygen species (ROS), and inhibiting the expression of caspase-3 and AIF in cytoplasm...
October 15, 2017: Phytomedicine: International Journal of Phytotherapy and Phytopharmacology
https://www.readbyqxmd.com/read/28861421/the-role-of-reactive-oxygen-species-in-myocardial-redox-signaling-and-regulation
#10
REVIEW
Demetrios Moris, Michael Spartalis, Eleni Tzatzaki, Eleftherios Spartalis, Georgia-Sofia Karachaliou, Andreas S Triantafyllis, Georgios I Karaolanis, Diamantis I Tsilimigras, Stamatios Theocharis
Reactive oxygen species (ROS) are subcellular messengers in gene regulatory and signal transduction pathways. In pathological situations, ROS accumulate due to excessive production or insufficient degradation, leading to oxidative stress (OS). OS causes oxidation of DNA, membranes, cellular lipids, and proteins, impairing their normal function and leading ultimately to cell death. OS in the heart is increased in response to ischemia/reperfusion, hypertrophy, and heart failure. The concentration of ROS is determined by their rates of production and clearance by antioxidants...
August 2017: Annals of Translational Medicine
https://www.readbyqxmd.com/read/28802666/humanin-directly-protects-cardiac-mitochondria-against-dysfunction-initiated-by-oxidative-stress-by-decreasing-complex-i-activity
#11
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
#12
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...
November 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
#13
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
#14
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)...
December 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
#15
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
#16
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...
November 2017: Biochimica et Biophysica Acta
https://www.readbyqxmd.com/read/28730272/mitochondria-as-a-target-of-cardioprotection-in-models-of-preconditioning
#17
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...
October 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
#18
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
#19
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...
September 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
#20
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
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