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heart and ischemia and mitochondria

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https://www.readbyqxmd.com/read/29777709/amelioration-of-myocardial-ischemia-reperfusion-injury-by-sirt4-involves-mitochondrial-protection-and-reduced-apoptosis
#1
Guangwei Zeng, Hui Liu, Haiyan Wang
Apoptosis and mitochondria dysfunction are key contributors to myocardial ischemia-reperfusion (MI-R) injury. SIRT4, a mitochondrial-localized sirtuin, controls cellular energy metabolism and stress response, and is abundantly present in the heart, however, its role in MI-R injury is not clear. In the current study, we demonstrate that SIRT4 is downregulated in cardiomyocytes both in vitro and in vivo models after MI-R. Functionally, SIRT4 overexpression decreases myocardial infarct size and serum creatine phosphokinase (CPK) level, and vice versa, SIRT4 depletion by siRNA increases myocardial infarct size and serum CPK level...
May 16, 2018: Biochemical and Biophysical Research Communications
https://www.readbyqxmd.com/read/29770298/mitochondrial-transplantation-applications-for-pediatric-patients-with-congenital-heart-disease
#2
REVIEW
Sitaram M Emani, James D McCully
Mitochondrial transplantation refers to transplantation of respiratory competent mitochondria from healthy tissue into tissues injured by ischemia and reperfusion. This technique has been utilized for recovery of myocardial dysfunction in pediatric patients. The preclinical experience and initial patient experience with this technique are reviewed in this article. Initial experience is with pediatric patients undergoing extracorporeal membrane oxygenation support following myocardial ischemia and reperfusion...
April 2018: Translational Pediatrics
https://www.readbyqxmd.com/read/29748710/critical-role-of-angiotensin-ii-type-2-receptors-in-the-control-of-mitochondrial-and-cardiac-function-in-angiotensin-ii-preconditioned-rat-hearts
#3
Rebeca E Nuñez, Sabzali Javadov, Nelson Escobales
Angiotensin II preconditioning (APC) involves an angiotensin II type 1 receptor (AT1-R)-dependent translocation of PKCε and survival kinases to the mitochondria leading to cardioprotection after ischemia-reperfusion (IR). However, the role that mitochondrial AT1-Rs and angiotensin II type 2 receptors (AT2-Rs) play in APC is unknown. We investigated whether pretreatment of Langendorff-perfused rat hearts with losartan (L, AT1-R blocker), PD 123,319 (PD, AT2-R blocker), or their combination (L + PD) affects mitochondrial AT1-R, AT2-R, PKCε, PKCδ, Akt, PKG-1, MAPKs (ERK1/2, JNK, p38), mitochondrial respiration, cardiac function, and infarct size (IS)...
May 10, 2018: Pflügers Archiv: European Journal of Physiology
https://www.readbyqxmd.com/read/29743240/control-of-mitochondrial-superoxide-production-by-reverse-electron-transport-at-complex-i
#4
Ellen L Robb, Andrew R Hall, Tracy A Prime, Simon Eaton, Marten Szibor, Carlo Viscomi, Andrew M James, Michael P Murphy
The generation of mitochondrial superoxide (O2 •- ) by reverse electron transport (RET) at complex I causes oxidative damage in pathologies such as ischemia reperfusion injury, but also provides the precursor to H2 O2 production in physiological mitochondrial redox signaling. Here, we quantified the factors that determine mitochondrial O2 •- production by RET in isolated heart mitochondria. Measuring mitochondrial H2 O2 production at a range of Δp values and for several CoQ and NADH pool redox states obtained with the uncoupler p-trifluoromethoxyphenylhydrazone, we show that O2 •- production by RET responds to changes in O2 concentration, the magnitude of the proton-motive force (Δp), and the redox states of the coenzyme Q (CoQ) and NADH pools...
May 9, 2018: Journal of Biological Chemistry
https://www.readbyqxmd.com/read/29701696/estrogen-and-or-estrogen-receptor-%C3%AE-inhibits-bnip3-induced-apoptosis-and-autophagy-in-h9c2-cardiomyoblast-cells
#5
Bih-Cheng Chen, Yi-Jiun Weng, Marthandam Asokan Shibu, Chien-Kuo Han, Yueh-Sheng Chen, Chia-Yao Shen, Yueh-Min Lin, Vijaya Padma Viswanadha, Hsin-Yueh Liang, Chih-Yang Huang
The process of autophagy in heart cells maintains homeostasis during cellular stress such as hypoxia by removing aggregated proteins and damaged organelles and thereby protects the heart during the times of starvation and ischemia. However, autophagy can lead to substantial cell death under certain circumstances. BCL2/adenovirus E1B 19 kDa protein-interacting protein 3 (BNIP3), a hypoxia-induced marker, has been shown to induce both autophagy and apoptosis. A BNIP3-docked organelle, e.g., mitochondria, also determines whether autophagy or apoptosis will take place...
April 26, 2018: International Journal of Molecular Sciences
https://www.readbyqxmd.com/read/29605530/zinc-improves-mitochondrial-respiratory-function-and-prevents-mitochondrial-ros-generation-at-reperfusion-by-phosphorylating-stat3-at-ser-727
#6
Ge Zhang, Mingwei Sheng, Jiannan Wang, Tianming Teng, Yuemin Sun, Qing Yang, Zhelong Xu
Serine 727 (Ser727 ) phosphorylation of STAT3 plays a role in the regulation of mitochondrial respiration. This study aimed to test if zinc could regulate mitochondrial respiration through phosphorylation of STAT3 at Ser727 in the setting of ischemia/reperfusion in the heart. Under normoxic conditions, treatment of isolated rat hearts with ZnCl2 increased cytosolic STAT3 phosphorylation at Ser727 followed by phospho-STAT3 translocation to mitochondria. In isolated rat hearts subjected to 30 min regional ischemia followed by 20 min of reperfusion, ZnCl2 given 5 min before the onset of reperfusion also increased mitochondrial phospho-STAT3...
March 29, 2018: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/29593106/ablation-of-the-stress-protease-oma1-protects-against-heart-failure-in-mice
#7
Rebeca Acin-Perez, Ana Victoria Lechuga-Vieco, Maria Del Mar Muñoz, Rocío Nieto-Arellano, Carlos Torroja, Fátima Sánchez-Cabo, Concepción Jiménez, Andrés González-Guerra, Isabel Carrascoso, Cristiane Benincá, Pedro M Quiros, Carlos López-Otín, José María Castellano, Jesús Ruíz-Cabello, Luis Jesús Jiménez-Borreguero, José Antonio Enríquez
Heart failure (HF) is a major health and economic burden in developed countries. It has been proposed that the pathogenesis of HF may involve the action of mitochondria. We evaluate three different mouse models of HF: tachycardiomyopathy, HF with preserved left ventricular (LV) ejection fraction (LVEF), and LV myocardial ischemia and hypertrophy. Regardless of whether LVEF is preserved, our results indicate that the three models share common features: an increase in mitochondrial reactive oxygen species followed by ultrastructural alterations in the mitochondrial cristae and loss of mitochondrial integrity that lead to cardiomyocyte death...
March 28, 2018: Science Translational Medicine
https://www.readbyqxmd.com/read/29576852/zp2495-protects-against-myocardial-ischemia-reperfusion-injury-in-diabetic-mice-through-improvement-of-cardiac-metabolism-and-mitochondrial-function-the-possible-involvement-of-ampk-foxo3a-signal-pathway
#8
Shuang Li, Hao Wu, Dong Han, Mingming Zhang, Na Li, Weihua Yu, Dongdong Sun, Zhongchan Sun, Sai Ma, Erhe Gao, Congye Li, Min Shen, Feng Cao
Coronary heart disease patients with type 2 diabetes were subject to higher vulnerability for cardiac ischemia-reperfusion (I/R) injury. This study was designed to evaluate the impact of ZP2495 (a glucagon-GLP-1 dual-agonist) on cardiac function and energy metabolism after myocardial I/R injury in db/db mice with a focus on mitochondrial function. C57BLKS/J-lepr+ /lepr+ (BKS) and db/db mice received 4-week treatment of glucagon, ZP131 (GLP-1 receptor agonist), or ZP2495, followed by cardiac I/R injury. The results showed that cardiac function, cardiac glucose metabolism, cardiomyocyte apoptosis, cardiac mitochondrial morphology, and energetic transition were improved or ameliorated by ZP2495 to a greater extent than that of glucagon and ZP131...
2018: Oxidative Medicine and Cellular Longevity
https://www.readbyqxmd.com/read/29569956/humoral-transfer-and-intra-myocardial-signal-transduction-of-protection-by-remote-ischemic-perconditioning-in-pigs-rats-and-mice
#9
Andreas Skyschally, Petra Kleinbongard, Helmut Raphael Lieder, Nilguen Gedik, Leanda Stoian, Georgios Amanakis, Etienne Elbers, Gerd Heusch
Remote ischemic perconditioning during ongoing myocardial ischemia (RPER), reduces infarct size. The signal transduction of RPER's cardioprotection is still largely unknown. Anesthetized pigs were therefore subjected to RPER by 4×5 min/5 min hindlimb ischemia/reperfusion during 60 min coronary occlusion before 3 h reperfusion. Pigs without RPER served as placebo (PLA). The phosphorylation of AKT and ERK (reperfusion injury salvage kinase [RISK] pathway), and STAT3 (survivor activating factor enhancement [SAFE] pathway) in the area at risk was determined by Western blot...
March 23, 2018: American Journal of Physiology. Heart and Circulatory Physiology
https://www.readbyqxmd.com/read/29554809/does-p53-inhibition-suppress-myocardial-ischemia-reperfusion-injury
#10
Toshiyuki Yano, Koki Abe, Masaya Tanno, Takayuki Miki, Atsushi Kuno, Tetsuji Miura, Charles Steenbergen
p53 is well known as a regulator of apoptosis and autophagy. In addition, a recent study showed that p53 is a modulator of the opening of the mitochondrial permeability transition pore (mPTP), a trigger event of necrosis, but the role of p53 in necrosis induced by myocardial ischemia-reperfusion (I/R) remains unclear. The aim of this study was to determine the role of p53 in acute myocardial I/R injury in perfused mouse hearts. In male C57BL6 mice between 12 and 15 weeks of age, 2 types of p53 inhibitors were used to suppress p53 function during I/R: pifithrin-α, an inhibitor of transcriptional functions of p53, and pifithrin-μ, an inhibitor of p53 translocation from the cytosol to mitochondria...
January 1, 2018: Journal of Cardiovascular Pharmacology and Therapeutics
https://www.readbyqxmd.com/read/29501746/partial-loss-of-complex-i-due-to-ndufs4-deficiency-augments-myocardial-reperfusion-damage-by-increasing-mitochondrial-superoxide-hydrogen-peroxide-production
#11
Nidhi Kuksal, Danielle Gardiner, Dake Qi, Ryan J Mailloux
Recent work has found that complex I is the sole source of reactive oxygen species (ROS) during myocardial ischemia-reperfusion (IR) injury. However, it has also been reported that heart mitochondria can also generate ROS from other sources in the respiratory chain and Krebs cycle. This study examined the impact of partial complex I deficiency due to selective loss of the Ndufs4 gene on IR injury to heart tissue. Mice heterozygous for NDUFS4 (NDUFS4+/-) did not display any significant changes in overall body or organ weight when compared to wild-type (WT) littermates...
March 25, 2018: Biochemical and Biophysical Research Communications
https://www.readbyqxmd.com/read/29496783/suppression-of-reactive-oxygen-species-generation-in-heart-mitochondria-from-anoxic-turtles-the-role-of-complex-i-s-nitrosation
#12
Amanda Bundgaard, Andrew M James, William Joyce, Michael P Murphy, Angela Fago
Freshwater turtles ( Trachemys scripta ) are among the very few vertebrates capable of tolerating severe hypoxia and re-oxygenation without suffering from damage to the heart. As myocardial ischemia and reperfusion causes a burst of mitochondrial reactive oxygen species (ROS) in mammals, the question arises as to whether, and if so how, this ROS burst is prevented in the turtle heart. We find that heart mitochondria isolated from turtles acclimated to anoxia produce less ROS than mitochondria from normoxic turtles when consuming succinate...
April 25, 2018: Journal of Experimental Biology
https://www.readbyqxmd.com/read/29416739/protective-role-of-stvna-in-myocardial-ischemia-reperfusion-injury-by-inhibiting-mitochondrial-fission
#13
Xiaoou Sun, Yingying Yang, Yanxiang Xie, Xingjuan Shi, Lijie Huang, Wen Tan
It has been reported that isosteviol, a widely known sweeteners, can protect against myocardial ischemia-reperfusion (IR) injury in isolated guinea pig heart. Here, we aim to confirm the cardioprotective effect of its sodium salt, isosteviol sodium (STVNa), against IR injury and its potential molecular mechanism in H9c2 cardiomyocytes. STVNa significantly improved cell viability, restored mitochondrial membrane potential, decreased cellular reactive oxygen species generation, and inhibited cell apoptosis. Furthermore, STVNa treatment changed the morphology of mitochondria from fragmented, discontinuous forms to normal elongated, tubular forms...
January 5, 2018: Oncotarget
https://www.readbyqxmd.com/read/29378951/holo-lipocalin-2-derived-siderophores-increase-mitochondrial-ros-and-impair-oxidative-phosphorylation-in-rat-cardiomyocytes
#14
Erfei Song, Sofhia V Ramos, Xiaojing Huang, Ying Liu, Amy Botta, Hye Kyoung Sung, Patrick C Turnbull, Michael B Wheeler, Thorsten Berger, Derek J Wilson, Christopher G R Perry, Tak W Mak, Gary Sweeney
Lipocalin-2 (Lcn2), a critical component of the innate immune response which binds siderophores and limits bacterial iron acquisition, can elicit spillover adverse proinflammatory effects. Here we show that holo-Lcn2 (Lcn2-siderophore-iron, 1:3:1) increases mitochondrial reactive oxygen species (ROS) generation and attenuates mitochondrial oxidative phosphorylation in adult rat primary cardiomyocytes in a manner blocked by N -acetyl-cysteine or the mitochondria-specific antioxidant SkQ1. We further demonstrate using siderophores 2,3-DHBA (2,3-dihydroxybenzoic acid) and 2,5-DHBA that increased ROS and reduction in oxidative phosphorylation are direct effects of the siderophore component of holo-Lcn2 and not due to apo-Lcn2 alone...
February 13, 2018: Proceedings of the National Academy of Sciences of the United States of America
https://www.readbyqxmd.com/read/29366934/sodium-thiosulfate-mediated-cardioprotection-against-myocardial-ischemia-reperfusion-injury-is-defunct-in-rat-heart-with-co-morbidity-of-vascular-calcification
#15
Sriram Ravindran, Kausthubh Ramachandran, Gino A Kurian
Sodium thiosulfate (STS) has shown promising effects in amelioration of myocardial ischemia-reperfusion injury (IR) in a rat model and is clinically useful in the treatment of chronic kidney disease (CKD) associated calciphylaxis. As the prevalence of cardiac complications is higher in CKD, we tested the effectiveness of STS in a rat model of adenine-induced vascular calcification and subjected the heart to IR. We observed an increased infarct size (29%) by TTC staining, lactate dehydrogenase (54%) and creatine kinase (32%) release in the coronary perfusate and altered hemodynamics compared to a normal rat treated with STS and subjected to IR...
April 2018: Biochimie
https://www.readbyqxmd.com/read/29362227/down-syndrome-critical-region-1-gene-rcan1-helps-maintain-a-more-fused-mitochondrial-network
#16
Valentina M Parra, Francisco Altamirano, Carolina P Hernández-Fuentes, Dan Tong, Viktoriia Kyrychenko, David Rotter, Zully R Pedrozo, Joseph A Hill, Veronica Eisner, Sergio Lavandero, Jay W Schneider, Beverly A Rothermel
<u>Rationale:</u> The Regulator of Calcineurin 1 (RCAN1) inhibits calcineurin (CN), a Ca2+ -activated protein phosphatase important in cardiac remodeling. In humans, RCAN1 is located on chromosome 21 in proximity to the "Down syndrome critical region." The hearts and brains of Rcan1 KO mice are more susceptible to damage from ischemia/reperfusion (I/R), however, the underlying cause is not known. <u>Objective:</u> Mitochondria are key mediators of I/R damage. The goal of these studies was to determine the impact of RCAN1 on mitochondrial dynamics and function...
January 23, 2018: Circulation Research
https://www.readbyqxmd.com/read/29351463/intermediary-metabolism-and-fatty-acid-oxidation-novel-targets-of-electron-transport-chain-driven-injury-during-ischemia-and-reperfusion
#17
Qun Chen, Masood Younus, Jeremy Thompson, Ying Hu, John M Hollander, Edward J Lesnefsky
Cardiac ischemia-reperfusion (I/R) damages the electron transport chain (ETC), causing mitochondrial and cardiomyocyte injury. Reversible blockade of the ETC at complex I during ischemia protects the ETC and decreases cardiac injury. In the present study, we used an unbiased proteomic approach to analyze the extent of ETC-driven mitochondrial injury during I/R. Isolated-perfused mouse (C57BL/6) hearts underwent 25-min global ischemia (37°C) and 30-min reperfusion. In treated hearts, amobarbital (2 mM) was given for 1 min before ischemia to rapidly and reversibly block the ETC at complex I...
April 1, 2018: American Journal of Physiology. Heart and Circulatory Physiology
https://www.readbyqxmd.com/read/29346115/mitochondrial-dysfunction-a-key-player-in-the-pathogenesis-of-cardiovascular-diseases-linked-to-air-pollution
#18
REVIEW
Sri Rahavi Boovarahan, Gino A Kurian
Air pollution has become an environmental burden with regard to non-communicable diseases, particularly heart disease. It has been reported that air pollution can accelerate the development of heart failure and atrial fibrillation. Air pollutants encompass various particulate matters (PMs), which change the blood composition and heart rate and eventually leads to cardiac failure by triggering atherosclerotic plaque ruptures or by developing irreversible ischemia. A series of major epidemiological and observational studies have established the noxious effect of air pollutants on cardiovascular diseases (CVD), but the underlying molecular mechanisms of its susceptibility and the pathological disease events remain largely elusive and are predicted to be initiated in the cell organelle...
January 18, 2018: Reviews on Environmental Health
https://www.readbyqxmd.com/read/29295576/intracellular-renin-inhibits-mitochondrial-permeability-transition-pore-via-activated-mitochondrial-extracellular-signal-regulated-kinase-erk-1-2-during-ischemia-in-diabetic-hearts
#19
Terumori Satoh, Masao Saotome, Hideki Katoh, Daishi Nonaka, Prottoy Hasan, Hideharu Hayashi, Yuichiro Maekawa
Although beneficial effects of non-secreting intracellular renin (ns-renin) against ischemia have been reported, the precise mechanism remains unclear. In this study, we investigated the roles of ns-renin and mitochondrial extracellular signal-related kinase (ERK) 1/2 on mitochondrial permeability transition pore (mPTP) opening during ischemia in diabetes mellitus (DM) hearts. When isolated hearts from Wistar rats (non-DM hearts) and Goto-Kakizaki rats (DM hearts) were subjected to ischemia for 70 min by left anterior descending coronary artery ligation, DM hearts exhibited higher left ventricular (LV) developed pressure and lower LV end-diastolic pressure than non-DM hearts, suggesting ischemic resistance...
December 25, 2017: International Journal of Molecular Sciences
https://www.readbyqxmd.com/read/29234096/transit-and-integration-of-extracellular-mitochondria-in-human-heart-cells
#20
Douglas B Cowan, Rouan Yao, Jerusha K Thedsanamoorthy, David Zurakowski, Pedro J Del Nido, James D McCully
Tissue ischemia adversely affects the function of mitochondria, which results in impairment of oxidative phosphorylation and compromised recovery of the affected organ. The impact of ischemia on mitochondrial function has been extensively studied in the heart because of the morbidity and mortality associated with injury to this organ. As conventional methods to preserve cardiac cell viability and contractile function following ischemia are limited in their efficacy, we developed a unique approach to protect the heart by transplanting respiration-competent mitochondria to the injured region...
December 12, 2017: Scientific Reports
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