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https://www.readbyqxmd.com/read/29449571/an-in-silico-argument-for-mitochondrial-microrna-as-a-determinant-of-primary-non-function-in-liver-transplantation
#1
Shirin Elizabeth Khorsandi, Siamak Salehi, Miriam Cortes, Hector Vilca-Melendez, Krishna Menon, Parthi Srinivasan, Andreas Prachalias, Wayel Jassem, Nigel Heaton
Mitochondria have their own genomic, transcriptomic and proteomic machinery but are unable to be autonomous, needing both nuclear and mitochondrial genomes. The aim of this work was to use computational biology to explore the involvement of Mitochondrial microRNAs (MitomiRs) and their interactions with the mitochondrial proteome in a clinical model of primary non function (PNF) of the donor after cardiac death (DCD) liver. Archival array data on the differential expression of miRNA in DCD PNF was re-analyzed using a number of publically available computational algorithms...
February 15, 2018: Scientific Reports
https://www.readbyqxmd.com/read/29428024/effect-of-systemic-triphenylphosphonium-on-organ-function-and-oxidative-stress
#2
Rebecca D Powell, Donna A Goodenow, A Britton Christmas, Iain H Mckillop, Susan L Evans
Conditions of systemic stress can lead to increased reactive oxygen species production, mitochondrial dysfunction, systemic inflammation, and multiorgan dysfunction. Triphenylphosphonium (TPP+) is a lipophilic cation used to target therapeutics to mitochondria. We sought to determine the effects of TPP+ on mitochondrial integrity. Male rats were anesthetized and TPP+ (5 mg/kg) or vehicle (saline) was administered intravenously 30-minutes after anesthesia initiation and intraperitoneally (20 mg/kg) 60-minutes later...
January 1, 2018: American Surgeon
https://www.readbyqxmd.com/read/29424033/mitochondrial-dysfunction-in-human-skeletal-muscle-biopsies-of-lipid-storage-disorder
#3
B Debashree, Manish Kumar, T S Keshava Prasad, Archana Natarajan, Rita Christopher, A Nalini, P S Bindu, N Gayathri, M M Srinivas Bharath
Mitochondria regulate the balance between lipid metabolism and storage in the skeletal muscle. Altered lipid transport, metabolism and storage influence the bioenergetics, redox status and insulin signalling contributing to cardiac and neurological diseases. Lipid storage disorders (LSDs) are neurological disorders which entail intramuscular lipid accumulation and impaired mitochondrial bioenergetics in the skeletal muscle causing progressive myopathy with muscle weakness. However, the mitochondrial changes including molecular events associated with impaired lipid storage have not been completely understood in the human skeletal muscle...
February 9, 2018: Journal of Neurochemistry
https://www.readbyqxmd.com/read/29421236/mitoq-improves-mitochondrial-dysfunction-in-heart-failure-induced-by-pressure-overload
#4
Rogério Faustino Ribeiro Junior, Erinne Rose Dabkowski, Kadambari Chandra Shekar, Kelly A O Connell, Peter A Hecker, Michael P Murphy
Heart failure remains a major public-health problem with an increase in the number of patients worsening from this disease. Despite current medical therapy, the condition still has a poor prognosis. Heart failure is complex but mitochondrial dysfunction seems to be an important target to improve cardiac function directly. Our goal was to analyze the effects of MitoQ (100 µM in drinking water) on the development and progression of heart failure induced by pressure overload after 14 weeks. The main findings are that pressure overload-induced heart failure in rats decreased cardiac function in vivo that was not altered by MitoQ...
February 1, 2018: Free Radical Biology & Medicine
https://www.readbyqxmd.com/read/29420962/activation-of-serine-one-carbon-metabolism-by-calcineurin-a%C3%AE-1-reduces-myocardial-hypertrophy-and-improves-ventricular-function
#5
Laura Padrón-Barthe, María Villalba-Orero, Jesús M Gómez-Salinero, Rebeca Acín-Pérez, Sara Cogliati, Marina López-Olañeta, Paula Ortiz-Sánchez, Elena Bonzón-Kulichenko, Jesús Vázquez, Pablo García-Pavía, Nadia Rosenthal, José Antonio Enríquez, Enrique Lara-Pezzi
BACKGROUND: In response to pressure overload, the heart develops ventricular hypertrophy that progressively decompensates and leads to heart failure. This pathological hypertrophy is mediated, among others, by the phosphatase calcineurin and is characterized by metabolic changes that impair energy production by mitochondria. OBJECTIVES: The authors aimed to determine the role of the calcineurin splicing variant CnAβ1 in the context of cardiac hypertrophy and its mechanism of action...
February 13, 2018: Journal of the American College of Cardiology
https://www.readbyqxmd.com/read/29408395/the-beneficial-role-of-exercise-in-mitigating-doxorubicin-induced-mitochondrionopathy
#6
REVIEW
I Marques-Aleixo, E Santos-Alves, P J Oliveira, P I Moreira, J Magalhães, A Ascensão
Doxorubicin (DOX) is a widely used antineoplastic agent for a wide range of cancers, including hematological malignancies, soft tissue sarcomas and solid tumors. However, DOX exhibits a dose-related toxicity that results in life-threatening cardiomyopathy. In addition to the heart, there is evidence that DOX toxicity extends to other organs. This general toxicity seems to be related to mitochondrial network structural, molecular and functional impairments. Several countermeasures for these negative effects have been proposed, being physical exercise, not only one of the most effective non-pharmacologic strategy but also widely recommended as booster against cancer-related fatigue...
February 2, 2018: Biochimica et Biophysica Acta
https://www.readbyqxmd.com/read/29398015/mitochondrial-oxidative-stress-and-cardiac-ageing
#7
Beatriz Martín-Fernández, Ricardo Gredilla
According with different international organizations, cardiovascular diseases are becoming the first cause of death in western countries. Although exposure to different risk factors, particularly those related to lifestyle, contribute to the etiopathogenesis of cardiac disorders, the increase in average lifespan and aging are considered major determinants of cardiac diseases events. Mitochondria and oxidative stress have been pointed out as relevant factors both in heart aging and in the development of cardiac diseases such as heart failure, cardiac hypertrophy and diabetic cardiomyopathy...
February 2, 2018: Clínica e Investigación en Arteriosclerosis
https://www.readbyqxmd.com/read/29388469/akap1-genetic-deletion-increases-the-severity-of-hyperoxia-induced-acute-lung-injury-in-mice
#8
Venkata R Narala, Jutaro Fukumoto, Helena Hernández-Cuervo, Sahebgowda Sidramagowda Patil, Sudarshan Krishnamurthy, Mason Breitzig, Lakshmi Galam, Ramani Soundararajan, Richard F Lockey, Narasaiah Kolliputi
Critically ill patients are commonly treated with high levels of oxygen, hyperoxia, for prolonged periods of time. Unfortunately, extended exposure to hyperoxia can exacerbate respiratory failure and lead to a high mortality rate. Mitochondrial A-kinase anchoring protein (Akap) has been shown to regulate mitochondrial function. It has been reported that, under hypoxic conditions, Akap121 undergoes proteolytic degradation and promotes cardiac injury. However, the role of Akap1 in hyperoxia-induced acute lung injury (ALI) is largely unknown...
February 1, 2018: American Journal of Physiology. Lung Cellular and Molecular Physiology
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
#9
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...
January 20, 2018: Biochimie
https://www.readbyqxmd.com/read/29362227/down-syndrome-critical-region-1-gene-rcan1-helps-maintain-a-more-fused-mitochondrial-network
#10
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
Rationale: 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. Objective: 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
#11
Qun Chen, Masood S Younus, Jeremy Thompson, Ying Hu, John M Hollander, Edward J Lesnefsky
BACKGROUND: Cardiac ischemia-reperfusion (IR) 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 IR. METHODS: Isolated-perfused mouse (C57BL/6) hearts underwent 25 min global ischemia (37{degree sign}C) and 30 min reperfusion...
December 29, 2017: American Journal of Physiology. Heart and Circulatory Physiology
https://www.readbyqxmd.com/read/29348263/phosphoinositide-3-kinase-gamma-inhibition-protects-from-anthracycline-cardiotoxicity-and-reduces-tumor-growth
#12
Mingchuan Li, Valentina Sala, Maria Chiara De Santis, James Cimino, Paola Cappello, Nicola Pianca, Anna Di Bona, Jean Piero Margaria, Miriam Martini, Edoardo Lazzarini, Flora Pirozzi, Luca Rossi, Irene Franco, Julia Bornbaum, Jacqueline Heger, Susanne Rohrbach, Alessia Perino, Carlo G Tocchetti, Braulio H F Lima, Mauro M Teixeira, Paolo E Porporato, Rainer Schulz, Annalisa Angelini, Marco Sandri, Pietro Ameri, Sebastiano Sciarretta, Roberto César P Lima-Júnior, Marco Mongillo, Tania Zaglia, Fulvio Morello, Francesco Novelli, Emilio Hirsch, Alessandra Ghigo
Background -Anthracyclines, such as doxorubicin (DOX), are potent anti-cancer agents for the treatment of solid tumors and hematological malignancies. However, their clinical use is hampered by cardiotoxicity. This study sought to investigate the role of PI3Kγ in DOX-induced cardiotoxicity and the potential cardio-protective and anti-cancer effects of PI3Kγ inhibition. Methods -Mice expressing a kinase-inactive PI3Kγ or receiving PI3Kγ selective inhibitors were subjected to chronic DOX treatment. Cardiac function was analyzed by echocardiography and DOX-mediated signaling was assessed in whole hearts or in isolated cardiomyocytes...
January 18, 2018: Circulation
https://www.readbyqxmd.com/read/29346115/mitochondrial-dysfunction-a-key-player-in-the-pathogenesis-of-cardiovascular-diseases-linked-to-air-pollution
#13
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/29344913/cardiac-basal-autophagic-activity-and-increased-exercise-capacity
#14
Fang-Hui Li, Tao Li, Ying-Min Su, Jing-Yi Ai, Rui Duan, Timon Cheng-Yi Liu
To investigate whether high-intensity interval training (HIIT) and continuous moderate-intensity training (CMT) have different impacts on exercise performance and cardiac function and to determine the influence of these exercise protocols on modulating basal autophagy in the cardiac muscle of rats. Rats were assigned to three groups: sedentary control (SC), CMT, and HIIT. Total exercise volume and mean intensity were matched between the two protocols. After a 10-week training program, rats were evaluated for exercise performance, including exercise tolerance and grip strength...
January 17, 2018: Journal of Physiological Sciences: JPS
https://www.readbyqxmd.com/read/29317051/the-end-stage-failing-human-myocardium-where-changes-in-ultrastructure-of-human-cardiac-muscle-cells-do-not-appear-to-dictate-clinical-outcomes
#15
Ivan Varga, Paulina Galfiova, Andrea Gazova, Tomas Barczi, Stefan Polak, Lubos Danisovic, Michal Hulman, Jan Kyselovic
Heart failure is the end stage of cardiovascular abnormalities. Studies have primarily focused on the functional changes of cardiomyocytes in the failing heart from different animal models with very little information in the human condition. In addition little is known about the ultrastructural changes that proceed in cardiomyocytes in route to failure. The aim of this study was to examine the ultrastructural changes in the myocardium of human with end-stage heart failure. Left ventricular myocardial tissue samples from 7 patients with end-stage heart failure were examined with transmission and scanning electron microscopy...
January 2018: Medical Hypotheses
https://www.readbyqxmd.com/read/29314656/mammalian-target-of-rapamycin-inhibition-attenuates-myocardial-ischaemia-reperfusion-injury-in-hypertrophic-heart
#16
Lei-Lei Ma, Xin Ma, Fei-Juan Kong, Jun-Jie Guo, Hong-Tao Shi, Jian-Bing Zhu, Yun-Zeng Zou, Jun-Bo Ge
Pathological cardiac hypertrophy aggravated myocardial infarction and is causally related to autophagy dysfunction and increased oxidative stress. Rapamycin is an inhibitor of serine/threonine kinase mammalian target of rapamycin (mTOR) involved in the regulation of autophagy as well as oxidative/nitrative stress. Here, we demonstrated that rapamycin ameliorates myocardial ischaemia reperfusion injury by rescuing the defective cytoprotective mechanisms in hypertrophic heart. Our results showed that chronic rapamycin treatment markedly reduced the phosphorylated mTOR and ribosomal protein S6 expression, but not Akt in both normal and aortic-banded mice...
January 4, 2018: Journal of Cellular and Molecular Medicine
https://www.readbyqxmd.com/read/29313986/protein-kinase-d-activation-induces-mitochondrial-fragmentation-and-dysfunction-in-cardiomyocytes
#17
Bong Sook Jhun, Jin O-Uchi, Stephanie M Adaniya, Tomas J Mancini, Jessica L Cao, Michelle E King, Amy K Landi, Hanley Ma, Milla Shin, Donqin Yang, Xiaole Xu, Yisang Yoon, Gaurav Choudhary, Richard T Clements, Ulrike Mende, Shey-Shing Sheu
Regulation of mitochondrial morphology is crucial for the maintenance of physiological functions in many cell types including cardiomyocytes. Small and fragmented mitochondria are frequently observed in pathological condition, but it is still unclear which cardiac signalling pathway is responsible for regulating the abnormal mitochondrial morphology in cardiomyocytes. Here we demonstrate that a downstream kinase of Gq -protein coupled receptor (Gq PCR) signalling, protein kinase D (PKD), mediates pathophysiological modifications in mitochondrial morphology and function, which consequently contribute to the activation of apoptotic signalling...
January 5, 2018: Journal of Physiology
https://www.readbyqxmd.com/read/29306791/empagliflozin-rescues-diabetic-myocardial-microvascular-injury-via-ampk-mediated-inhibition-of-mitochondrial-fission
#18
Hao Zhou, Shuyi Wang, Pingjun Zhu, Shunying Hu, Yundai Chen, Jun Ren
Impaired cardiac microvascular function contributes to diabetic cardiovascular complications although effective therapy remains elusive. Empagliflozin, a sodium-glucose cotransporter 2 (SGLT2) inhibitor recently approved for treatment of type 2 diabetes, promotes glycosuria excretion and offers cardioprotective actions beyond its glucose-lowering effects. This study was designed to evaluate the effect of empagliflozin on cardiac microvascular injury in diabetes and the underlying mechanism involved with a focus on mitochondria...
December 30, 2017: Redox Biology
https://www.readbyqxmd.com/read/29285172/omega-3-polyunsaturated-fatty-acids-prevent-murine-dilated-cardiomyopathy-by-reducing-oxidative-stress-and-cardiomyocyte-apoptosis
#19
Qianxiao Li, Qin Yu, Rongmei Na, Baiting Liu
Mice that lacked manganese-superoxide dismutase (Mn-SOD) activity exhibited the typical pathology of dilated cardiomyopathy (DCM). The aim of the present study was to investigate the effect of supplementation with omega-3 polyunsaturated fatty acids (n-3 PUFA) on heart function and oxidative stress biomarkers in mice with DCM. In the present study, heart/muscle-specific Mn-SOD-deficient mice (H/M-Sod2-/-) were treated with n-3 PUFA (30 mg/kg/day) for 10 weeks, and the reactive oxygen species (ROS) production in their heart mitochondria and cardiac function was subsequently assessed...
December 2017: Experimental and Therapeutic Medicine
https://www.readbyqxmd.com/read/29284690/ampk%C3%AE-2-protects-against-the-development-of-heart-failure-by-enhancing-mitophagy-via-pink1-phosphorylation
#20
Bei Wang, Jiali Nie, Lujin Wu, Yangyang Hu, Zeng Wen, Lingli Dong, Ming-Hui Zou, Chen Chen, Dao Wen Wang
Rationale: Mitochondrial dysfunction plays an important role in heart failure (HF). However, the molecular mechanisms regulating mitochondrial functions via selective mitochondrial autophagy (mitophagy) are poorly understood. Objective: We sought to determine the role of AMP-activated protein kinase (AMPK) in selective mitophagy during HF. Methods and Results: An isoform shift from AMPKα2 to AMPKα1 was observed in failing-heart samples from HF patients and transverse aortic constriction (TAC)-induced mice, accompanied by decreased mitophagy and mitochondrial function...
December 28, 2017: Circulation Research
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