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heart and ischemia and mitochondria

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https://www.readbyqxmd.com/read/28323531/mitophagy-receptor-fundc1-regulates-mitochondrial-homeostasis-and-protects-the-heart-from-i-r-injury
#1
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 ageing-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-cardioprotective-effect-of-chronic-continuous-hypoxia-in-spontaneously-hypertensive-rats
#2
Jan Neckar, Anna Svatonova, Romana Weissova, Zdenek Drahota, Pavlina Zajickova, Iveta Brabcova, David Kolar, Petra Alanova, Jana Vasinova, Jan Silhavy, Marketa Hlavackova, Katerina Tauchmannova, Marie Milerova, Bohuslav Ostadal, Ludek Cervenka, Jitka Zurmanova, Martin Kalous, Olga Novakova, Jiri Novotny, Michal Pravenec, Frantisek Kolar
Mitochondria play an essential role in improved cardiac ischemic tolerance conferred by adaptation to chronic hypoxia. In the present study, we analyzed effects of continuous normobaric hypoxia (CNH) on mitochondrial functions, including the sensitivity of mitochondrial permeability transition pore (MPTP) to opening, and infarct size in hearts of spontaneously hypertensive rats (SHR) and in conplastic SHR-mtBN strain characterized by the selective replacement of the mitochondrial genome of SHR with that of more ischemia-resistant Brown Norway (BN) strain...
March 14, 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
#3
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
#4
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
#5
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
#6
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
#7
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
#8
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
#9
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
https://www.readbyqxmd.com/read/28242633/divergent-effects-of-mir-181-family-members-on-myocardial-function-through-protective-cytosolic-and-detrimental-mitochondrial-microrna-targets
#10
Samarjit Das, Mark Kohr, Brittany Dunkerly-Eyring, Dong I Lee, Djahida Bedja, Oliver A Kent, Anthony K L Leung, Jorge Henao-Mejia, Richard A Flavell, Charles Steenbergen
BACKGROUND: MicroRNA (miRNA) is a type of noncoding RNA that can repress the expression of target genes through posttranscriptional regulation. In addition to numerous physiologic roles for miRNAs, they play an important role in pathophysiologic processes affecting cardiovascular health. Previously, we reported that nuclear encoded microRNA (miR-181c) is present in heart mitochondria, and importantly, its overexpression affects mitochondrial function by regulating mitochondrial gene expression...
February 27, 2017: Journal of the American Heart Association
https://www.readbyqxmd.com/read/28239650/mitophagy-and-mitochondrial-biogenesis-in-atrial-tissue-of-patients-undergoing-heart-surgery-with-cardiopulmonary-bypass
#11
Allen M Andres, Kyle C Tucker, Amandine Thomas, David J R Taylor, David Sengstock, Salik M Jahania, Reza Dabir, Somayeh Pourpirali, Jamelle A Brown, David G Westbrook, Scott W Ballinger, Robert M Mentzer, Roberta A Gottlieb
Mitophagy occurs during ischemia/reperfusion (I/R) and limits oxidative stress and injury. Mitochondrial turnover was assessed in patients undergoing cardiac surgery involving cardiopulmonary bypass (CPB). Paired biopsies of right atrial appendage before initiation and after weaning from CPB were processed for protein analysis, mitochondrial DNA/nuclear DNA ratio (mtDNA:nucDNA ratio), mtDNA damage, mRNA, and polysome profiling. Mitophagy in the post-CPB samples was evidenced by decreased levels of mitophagy adapters NDP52 and optineurin in whole tissue lysate, decreased Opa1 long form, and translocation of Parkin to the mitochondrial fraction...
February 23, 2017: JCI Insight
https://www.readbyqxmd.com/read/28194639/ultrafine-particulate-matter-increases-cardiac-ischemia-reperfusion-injury-via-mitochondrial-permeability-transition-pore
#12
Nathan A Holland, Chad R Fraiser, Ruben C Sloan, Robert B Devlin, David A Brown, Christopher J Wingard
Ultrafine particulate matter (UFP) has been associated with increased cardiovascular morbidity and mortality. However, the mechanisms that drive PM-associated cardiovascular disease and dysfunction remain unclear. We examined the impact of oropharyngeal aspiration of 100 μg UFP from the Chapel Hill, NC, air shed in Sprague-Dawley rats on cardiac function, arrhythmogenesis, and cardiac ischemia/reperfusion (I/R) injury using a Langendorff working heart model. We found that exposure to UFP was capable of significantly exacerbating cardiac I/R injury without changing overall cardiac function or major changes in arrhythmogenesis...
February 13, 2017: Cardiovascular Toxicology
https://www.readbyqxmd.com/read/28191472/suppression-of-excessive-histone-deacetylases-activity-in-diabetic-hearts-attenuates-myocardial-ischemia-reperfusion-injury-via-mitochondria-apoptosis-pathway
#13
Yang Wu, Yan Leng, Qingtao Meng, Rui Xue, Bo Zhao, Liying Zhan, Zhongyuan Xia
Background. Histone deacetylases (HDACs) play a pivotal role in signaling modification and gene transcriptional regulation that are essential for cardiovascular pathophysiology. Diabetic hearts with higher HDACs activity were more vulnerable to myocardial ischemia/reperfusion (MI/R) injury compared with nondiabetic hearts. We are curious about whether suppression of excessive HDACs activity in diabetic heart protects against MI/R injury. Methods. Diabetic rats were subjected to 45 min of ischemia, followed by 3 h of reperfusion...
2017: Journal of Diabetes Research
https://www.readbyqxmd.com/read/28181692/irisin-plays-a-pivotal-role-to-protect-the-heart-against-ischemia-and-reperfusion-injury
#14
Hao Wang, Yu Tina Zhao, Shouyan Zhang, Patrycja M Dubielecka, Jianfeng Du, Naohiro Yano, Y Eugene Chin, Shougang Zhuang, Gangjian Qin, Ting C Zhao
Irisin, a newly identified hormone, is critical to modulating body metabolism, thermogenesis and reducing oxidative stresses. However, whether irisin protects the heart against myocardial ischemia and reperfusion (I/R) injury remains unknown. In this study, we determine the effect of irisin on myocardial I/R injury in the Langendorff perfused heart and cultured myocytes. Adult C57/BL6 mice were treated with irisin (100mg/kg) or vehicle for 30 minutes to elicit preconditioning. The isolated hearts were subjected to 30 min ischemia followed by 30 min reperfusion...
February 9, 2017: Journal of Cellular Physiology
https://www.readbyqxmd.com/read/28173848/inhibition-of-dynamin-related-protein-1-protects-against-myocardial-ischemia-reperfusion-injury-in-diabetic-mice
#15
Mingge Ding, Qianqian Dong, Zhenghua Liu, Zheng Liu, Yinxian Qu, Xing Li, Cong Huo, Xin Jia, Feng Fu, Xiaoming Wang
BACKGROUND: Many cardioprotective pharmacological agents failed to exert their protective effects in diabetic hearts subjected to myocardial ischemia/reperfusion (MI/R). Identify the molecular basis linking diabetes with MI/R injury is scientifically important and may provide effective therapeutic approaches. Dynamin-related protein 1 (Drp1)-mediated mitochondrial fission plays an important role in MI/R injury under non-diabetic conditions. Importantly, recent studies indicated that Drp1-mediated mitochondrial fission is enhanced in the myocardium of diabetic mice...
February 7, 2017: Cardiovascular Diabetology
https://www.readbyqxmd.com/read/28160133/cardioprotective-kinase-signaling-to-subsarcolemmal-and-interfibrillar-mitochondria-is-mediated-by-caveolar-structures
#16
Wylly Ramsés García-Niño, Francisco Correa, Julia Isabel Rodríguez-Barrena, Juan Carlos León-Contreras, Mabel Buelna-Chontal, Elizabeth Soria-Castro, Rogelio Hernández-Pando, José Pedraza-Chaverri, Cecilia Zazueta
The demonstration that caveolin-3 overexpression reduces myocardial ischemia/reperfusion injury and our own finding that multiprotein signaling complexes increase in mitochondria in association with caveolin-3 levels, led us to investigate the contribution of caveolae-driven extracellular signal-regulated kinases 1/2 (ERK1/2) on maintaining the function of cardiac mitochondrial subpopulations from reperfused hearts subjected to postconditioning (PostC). Rat hearts were isolated and subjected to ischemia/reperfusion and to PostC...
March 2017: Basic Research in Cardiology
https://www.readbyqxmd.com/read/28096195/the-multifunctional-mitochondrial-epac1-controls-myocardial-cell-death
#17
Loubina Fazal, Marion Laudette, Sílvia Paula-Gomes, Sandrine Pons, Caroline Conte, Florence Tortosa, Pierre Sicard, Yannis Sainte-Marie, Malik Bisserier, Olivier Lairez, Alexandre Lucas, Jérôme Roy, Bijan Ghaleh, Jeremy Fauconnier, Jeanne Mialet-Perez, Frank Lezoualc'h
RATIONALE: Although the second messenger cyclic AMP (cAMP) is physiologically beneficial in the heart, it largely contributes to cardiac disease progression when dysregulated. Current evidence suggests that cAMP is produced within mitochondria. However, mitochondrial cAMP signaling and its involvement in cardiac pathophysiology are far from being understood. OBJECTIVE: To investigate the role of mitochondrial exchange protein directly activated by cAMP 1 (MitEpac1) in ischemia/reperfusion (I/R) injury...
January 17, 2017: Circulation Research
https://www.readbyqxmd.com/read/28096168/sk-channel-enhancers-attenuate-ca2-dependent-arrhythmia-in-hypertrophic-hearts-by-regulating-mito-ros-dependent-oxidation-and-activity-of-ryr
#18
Tae Yun Kim, Radmila Terentyeva, Karim H F Roder, Weiyan Li, Man Liu, Ian Greener, Shanna Hamilton, Iuliia Polina, Kevin R Murphy, Richard T Clements, Samuel C Dudley, Gideon Koren, Bum-Rak Choi, Dmitry Terentyev
AIM: s: Plasmamembrane small conductance Ca<su2+p>-activated K<su+ p > (SK) channels were implicated in ventricular arrhythmias in infarcted and failing hearts. Recently, SK channels were detected in the mitochondria inner membrane (mSK), and their activation protected from acute ischemia-reperfusion injury by reducing intracellular levels of reactive oxygen species (ROS). We hypothesized that mSK play an important role in regulating mitochondrial function in chronic cardiac diseases...
January 17, 2017: Cardiovascular Research
https://www.readbyqxmd.com/read/28093764/pre-ischemic-mitochondrial-substrate-constraint-by-inhibition-of-malate-aspartate-shuttle-preserves-mitochondrial-function-after-ischemia-reperfusion
#19
Nichlas Riise Jespersen, Takashi Yokota, Nicolaj Brejnholt Støttrup, Andreas Bergdahl, Kim Bolther Paelestik, Jonas Agerlund Povlsen, Flemming Dela, Hans Erik Bøtker
Mitochondrial dysfunction plays a central role in ischemia-reperfusion (IR) injury. The pre-ischemic administration of aminooxyacetate (AOA), an inhibitor of the malate-aspartate shuttle (MAS), provides cardioprotection against IR injury, but the underlying mechanism remains unknown. We hypothesized that a transient inhibition of the MAS during ischemia and early reperfusion could preserve mitochondrial function at later phase of reperfusion in IR-injured heart to the same extent as ischemic preconditioning (IPC), which is a well-validated cardioprotective strategy against IR injury...
January 17, 2017: Journal of Physiology
https://www.readbyqxmd.com/read/28024940/a-new-flavonoid-glycoside-apg-isolated-from-clematis-tangutica-attenuates-myocardial-ischemia-reperfusion-injury-via-activating-pkc%C3%AE%C2%B5-signaling
#20
Yanrong Zhu, Shouyin Di, Wei Hu, Yingda Feng, Qing Zhou, Bing Gong, Xinlong Tang, Juntian Liu, Wei Zhang, Miaomiao Xi, Lin Jiang, Chao Guo, Jingyi Cao, Chongxi Fan, Zhiqiang Ma, Yang Yang, Aidong Wen
Clematis tangutica has been shown to be beneficial for the heart; however, the mechanism of this effectremains unknown. Apigenin-7-O-β-D-(-6″-p-coumaroyl)-glucopyranoside (APG) is a new flavonoid glycoside isolated from Clematis tangutica. This study investigates the effects of APG on myocardial ischemia/reperfusion (IR) injury (IRI). An IRI model of primary myocardial cells and mice was used in this study. Compared with the IR group, APG preconditioning is protective against IRI in primary myocardial cells and in mice hearts in a dose-dependent manner...
December 24, 2016: Biochimica et Biophysica Acta
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