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heart and ischemia and mitochondria

Wangde Dai, Elissa Cheung, Rick J Alleman, Justin B Perry, Mitchell E Allen, David A Brown, Robert A Kloner
PURPOSE: Dysfunctional mitochondria are considered to be the major source of intracellular reactive oxygen species and play a central role in the pathophysiology of myocardial ischemia/reperfusion. This study sought to determine effects of mitochondria-targeted cytoprotective peptide SBT-20 on myocardial infarct size in two different models of ischemia/reperfusion. METHODS: For in vivo studies, anesthetized Sprague Dawley rats were subjected to 30 min of coronary artery occlusion followed by 3 h of reperfusion...
October 17, 2016: Cardiovascular Drugs and Therapy
Marie N Hansen, Jon O Lundberg, Mariacristina Filice, Angela Fago, Nanna M G Christensen, Frank B Jensen
In mammals, treatment with low doses of nitrite have cytoprotective effects in ischemia/reperfusion events, due to nitric oxide formation and S-nitrosation of proteins. Interestingly, anoxia-tolerant lower vertebrates possess an intrinsic ability to increase intracellular [nitrite] during anoxia in tissues with high myoglobin and mitochondria contents, such as the heart. Here we test the hypothesis that red and white skeletal muscle develops different nitrite levels in crucian carp exposed to deep hypoxia and whether this correlates with myoglobin concentration...
October 14, 2016: Journal of Experimental Biology
Carola Schubert, Valeria Raparelli, Christina Westphal, Elke Dworatzek, George Petrov, Georgios Kararigas, Vera Regitz-Zagrosek
BACKGROUND: Estrogen improves cardiac recovery after ischemia/reperfusion (I/R) by yet incompletely understood mechanisms. Mitochondria play a crucial role in I/R injury through cytochrome c-dependent apoptosis activation. We tested the hypothesis that 17β-estradiol (E2) as well as a specific ERβ agonist improve cardiac recovery through estrogen receptor (ER)β-mediated mechanisms by reducing mitochondria-induced apoptosis and preserving mitochondrial integrity. METHODS: We randomized ovariectomized C57BL/6N mice 24h before I/R to pre-treatment with E2 or a specific ERβ agonist (ERβA)...
2016: Biology of Sex Differences
Ngonidzashe B Madungwe, Netanel F Zilberstein, Yansheng Feng, Jean C Bopassa
Reactive oxygen species (ROS) generation has been implicated in many pathologies including ischemia/reperfusion (I/R) injury. This led to multiple studies on antioxidant therapies to treat cardiovascular diseases but paradoxically, results have so far been mixed as ROS production can be beneficial as a signaling mechanism and in cardiac protection via preconditioning interventions. We investigated whether the differential impact of increased ROS in injury as well as in protection could be explained by their site of production on the mitochondrial electron transport chain...
2016: American Journal of Cardiovascular Disease
Qiang Li, Li Shen, Zhen Wang, Hai-Peng Jiang, Li-Xia Liu
OBJECTIVE: To determine the mechanism by which Tanshinone IIA (Tan IIA) relieves myocardial ischemia reperfusion injury (MIRI) in rats via the PI3K/Akt/mTOR signaling pathway. METHODS: Sprague-Dawley (SD) rats received an intravenous injection of Tan IIA and LY294002 and were divided into the sham, control (myocardial ischemia reperfusion), Tan-L (low-dose Tan IIA), Tan-H (high-dose Tan IIA), Tan-L+LY (low-dose Tan IIA+LY294002), Tan-H+LY (high-dose Tan IIA+LY294002) and LY (LY294002) groups...
September 16, 2016: Biomedicine & Pharmacotherapy, Biomédecine & Pharmacothérapie
Xiangwei Liu, Aijun Sun
Coronary heart disease is the leading cause of mortality and morbidity, incurring a major burden of medical care. Even with increasing application of emergent recanalization (PCI and CABG) therapy, ischemia and ischemic reperfusion injury remain as the dominant pathological process that damages cardiomyocytes. Mitochondrial Aldehyde dehydrogenase-2 (ALDH2) is a multifunctional enzyme catalyzing the oxidation of aldehydes. Accumulating data have shown that ALDH2 can help restore mitochondria function by eliminating toxic aldehyde and participating in cellular signaling important for cell adaption and survival...
September 12, 2016: Current Drug Targets
Lara Testai, Alice Marino, Ilaria Piano, Vincenzo Brancaleone, Kengo Tomita, Lorenzo Di Cesare Mannelli, Alma Martelli, Valentina Citi, Maria C Breschi, Roberto Levi, Claudia Gargini, Mariarosaria Bucci, Giuseppe Cirino, Carla Ghelardini, Vincenzo Calderone
The endogenous gasotransmitter hydrogen sulphide (H2S) is an important regulator of the cardiovascular system, particularly of myocardial function. Moreover, H2S exhibits cardioprotective activity against ischemia/reperfusion (I/R) or hypoxic injury, and is considered an important mediator of "ischemic preconditioning", through activation of mitochondrial potassium channels, reduction of oxidative stress, activation of the endogenous "anti-oxidant machinery" and limitation of inflammatory responses. Accordingly, H2S-donors, i...
September 9, 2016: Pharmacological Research: the Official Journal of the Italian Pharmacological Society
Sehwan Jang, Taber S Lewis, Corey Powers, Zaza Khuchua, Christopher P Baines, Peter Wipf, Sabzali Javadov
<b>Aims:</b> Mitochondrial supercomplexes (SCs) are the large supramolecular assembly of individual electron transport chain (ETC) complexes that apparently provide highly efficient ATP synthesis and reduce electron leakage and ROS production. Oxidative stress during cardiac ischemia-reperfusion (IR) can result in degradation of SCs through oxidation of cardiolipin. Also, IR induces calcium overload, and enhances reactive oxygen species (mitROS) in mitochondria that result in the opening of the non-selective permeability transition pores (PTP)...
September 7, 2016: Antioxidants & Redox Signaling
Mahsa Ranji, Mohammad Masoudi Motlagh, Fahimeh Salehpour, Reyhaneh Sepehr, James S Heisner, Ranjan K Dash, Amadou K S Camara
Oxidation of substrates to generate ATP in mitochondria is mediated by redox reactions of NADH and FADH2. Cardiac ischemia and reperfusion (IR) injury compromises mitochondrial oxidative phosphorylation. We hypothesize that IR alters the metabolic heterogeneity of mitochondrial redox state of the heart that is only evident in the 3-D optical cryoimaging of the perfused heart before, during, and after IR. The study involved four groups of hearts: time control (TC: heart perfusion without IR), global ischemia (Isch), global ischemia followed by reperfusion (IR) and TC with PCP (a mitochondrial uncoupler) perfusion...
2016: IEEE Journal of Translational Engineering in Health and Medicine
Paulina Brodek, Beata Olas
Hydrogen sulfide (H2S) is a signaling gasotransmitter, involved in different physiological and pathological processes. H2S regulates apoptosis, the cell cycle and oxidative stress. H2S exerts powerful effects on smooth muscle cells, endothelial cells, inflammatory cells, endoplasmic reticulum, mitochondria and nuclear transcription factors. H2S is known to be produced from L-cysteine, D-cysteine and L-homocysteine in the body. Four enzymes - cystathionine-b synthase (CBS), mercaptopyruvate sulfurtransferase (3-MST), cystathionine-γ lyase (CSE) and cysteine aminotransferase (CAT) - are involved in H2S synthesis...
2016: Postȩpy Higieny i Medycyny Doświadczalnej
Douglas B Cowan, Rouan Yao, Vamsidhar Akurathi, Erin R Snay, Jerusha K Thedsanamoorthy, David Zurakowski, Maria Ericsson, Ingeborg Friehs, Yaotang Wu, Sidney Levitsky, Pedro J Del Nido, Alan B Packard, James D McCully
We have previously shown that transplantation of autologously derived, respiration-competent mitochondria by direct injection into the heart following transient ischemia and reperfusion enhances cell viability and contractile function. To increase the therapeutic potential of this approach, we investigated whether exogenous mitochondria can be effectively delivered through the coronary vasculature to protect the ischemic myocardium and studied the fate of these transplanted organelles in the heart. Langendorff-perfused rabbit hearts were subjected to 30 minutes of ischemia and then reperfused for 10 minutes...
2016: PloS One
Russel J Reiter, Juan C Mayo, Dun-Xian Tan, Rosa M Sainz, Moises Alatorre-Jimenez, Lilian Qin
Melatonin is uncommonly effective in reducing oxidative stress under a remarkably large number of circumstances. It achieves this action via a variety of means: direct detoxification of reactive oxygen and reactive nitrogen species and indirectly by stimulating antioxidant enzymes while suppressing the activity of pro-oxidant enzymes. In addition to these well-described actions, melatonin also reportedly chelates transition metals, which are involved in the Fenton/Haber-Weiss reactions; in doing so, melatonin reduces the formation of the devastatingly toxic hydroxyl radical resulting in the reduction of oxidative stress...
October 2016: Journal of Pineal Research
Sung Ho Moon, David J Mancuso, Harold F Sims, Xinping Liu, Annie L Nguyen, Kui Yang, Shaoping Guan, Beverly Gibson Dilthey, Christopher M Jenkins, Carla J Weinheimer, Attila Kovacs, Dana Abendschein, Richard W Gross
Calcium-independent phospholipase A2γ (iPLA2γ) is a mitochondrial enzyme that produces lipid second messengers that facilitate opening of the mitochondrial permeability transition pore (mPTP) and contribute to the production of oxidized fatty acids in myocardium. To specifically identify the roles of iPLA2γ in cardiac myocytes, we generated cardiac myocyte-specific iPLA2γ knock-out (CMiPLA2γKO) mice by removing the exon encoding the active site serine (Ser-477). Hearts of CMiPLA2γKO mice exhibited normal hemodynamic function, glycerophospholipid molecular species composition, and normal rates of mitochondrial respiration and ATP production...
September 9, 2016: Journal of Biological Chemistry
Ayako Ishikita, Tetsuya Matoba, Gentaro Ikeda, Jun-Ichiro Koga, Yajing Mao, Kaku Nakano, Osamu Takeuchi, Junichi Sadoshima, Kensuke Egashira
BACKGROUND: Mitochondria-mediated cell death plays a critical role in myocardial ischemia-reperfusion (IR) injury. We hypothesized that nanoparticle-mediated drug delivery of mitochondrial division inhibitor 1 (Mdivi1) protects hearts from IR injury through inhibition of mitochondria outer membrane permeabilization (MOMP), which causes mitochondrial-mediated cell death. METHODS AND RESULTS: We formulated poly (lactic-co-glycolic acid) nanoparticles containing Mdivi1 (Mdivi1-NP)...
2016: Journal of the American Heart Association
Savitree T Charununtakorn, Nattayaporn Apaijai, Sasiwan Kerdphoo, Krekwit Shinlapawittayatorn, Siriporn C Chattipakorn, Nipon Chattipakorn
AIM: Myocardial reperfusion via the re-canalization of occluded coronary arteries is gold standard for the treatment of acute myocardial infarction. However, reperfusion itself can cause myocardial damage due to increased reactive oxygen species (ROS) production, a process known as ischemia/reperfusion (I/R) injury. Cardiac mitochondria are the major organelle of ROS production in the heart. Cardiac mitochondrial dysfunction caused by an increased ROS production can increase cardiac arrhythmia incidence, myocardial infarct size and cardiac dysfunction...
July 19, 2016: Cardiovascular Therapeutics
Yi Lu, Yi-Dong Wang, Xiao-Ya Wang, Han Chen, Zhe-Jun Cai, Mei-Xiang Xiang
SIRT3 belongs to a highly conserved protein family of histone deacetylases and it is rich in mitochondria. As acetyl-modification is one of the important post-translational modifications that prevail in the mitochondria, it is not surprising that SIRT3 plays a key regulatory role in this organelle. SIRT3 has a wide range of substrates that are involved in the physiological and pathological processes of oxidative stress, ischemia-reperfusion injury, mitochondrial metabolism homeostasis and cellular death. These pathophysiological processes are considered as the underlying mechanisms of diseases like cardiac hypertrophy, myocardial infarction and heart failure, indicating the potential roles of SIRT3 in cardiovascular diseases...
October 1, 2016: International Journal of Cardiology
Jing Wang, Hai-hua Wang, Ping-ping Zhou, Yu-xin Jiang
OBJECTIVE: To explore regulatory mechanism of Ginkgo-dipyridamolum (GD) for calcium homeostasis on cardioprotective effect during ischemia reperfusion injury in the isolated rat heart. METHODS: 40 male SD-rats were randomly divided into five groups (n = 8): normal control group (NC), ischemia reperfusion group (IR), GD precondition group (GD + IR), Nicardipine and GD precondition group( Nic + GD + IR), and LaCl3 and GD precondition group (LaCl, + GD +IR). The hearts of rats were isolated after anesthesia and performed to profuse with Langendorff equipment...
December 2015: Zhong Yao Cai, Zhongyaocai, Journal of Chinese Medicinal Materials
Zuolei Chen, Xuewei Zhang, Yingzhi Liu, Zhongkai Liu
BACKGROUND: The purpose of this study was to determine whether c-jun NH2 amino-terminal kinases (JNK) and p38 mitogen-activated protein kinases (MAPK) were involved in morphine postconditioning (MpostC). METHODS: The isolated rat hearts were randomly assigned into one of the following groups. Hearts in the time control (TC) group were constantly perfused for 105min. Hearts in the ischemia-reperfusion (I/R) group were subjected to 45 min of ischemia followed by 1 h of reperfusion...
2016: Cellular Physiology and Biochemistry
Kent Doi
Acute kidney injury (AKI) is a common complication in critically ill patients treated in intensive care units. Renal replacement therapy (RRT)-requiring AKI occurs in approximately 5-10% patients in intensive care unit and their mortality rate is unacceptably high (50-60%), despite sufficient control of uremia using remarkably advanced modern RRT techniques. This suggests that there are unrecognized organ interactions following AKI that could worsen the outcomes. Cardiorenal syndrome has been defined based on clinical observations that acute and chronic heart failure causes kidney injury and AKI and that chronic kidney disease worsens heart diseases...
June 16, 2016: Nephron
Harmen G Booij, Hongjuan Yu, Rudolf A De Boer, Cees W A van de Kolk, Bart van de Sluis, Jan M Van Deursen, Wiek H Van Gilst, Herman H W Silljé, B Daan Westenbrink
AIMS: A kinase interacting protein 1 (AKIP1) stimulates physiological growth in cultured cardiomyocytes and attenuates ischaemia/reperfusion (I/R) injury in ex vivo perfused hearts. We aimed to determine whether AKIP1 modulates the cardiac response to acute and chronic cardiac stresses in vivo. METHODS AND RESULTS: Transgenic mice with cardiac-specific overexpression of AKIP1 (AKIP1-TG) were created. AKIP1-TG mice and their wild-type (WT) littermates displayed similar cardiac structure and function...
August 1, 2016: Cardiovascular Research
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