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https://www.readbyqxmd.com/read/27930802/ap39-a-mitochondria-targeting-hydrogen-sulfide-h2-s-donor-protects-against-myocardial-reperfusion-injury-independently-of-salvage-kinase-signalling
#1
Qutuba G Karwi, Julia Bornbaum, Kerstin Boengler, Roberta Torregrossa, Matthew Whiteman, Mark E Wood, Rainer Schulz, Gary F Baxter
BACKGROUND AND PURPOSE: H2 S protects myocardium against ischaemia-reperfusion injury. This protection may involve the cytosolic reperfusion injury salvage kinase (RISK) pathway, but direct effects on mitochondrial function are possible. Here, we investigated the potential cardioprotective effect of mitochondria-specific H2 S donor, AP39, at reperfusion against ischaemia/reperfusion injury. EXPERIMENTAL APPROACH: Anaesthetised rats underwent myocardial (30 min ischaemia/120 min reperfusion) with randomisation to receive interventions prior to reperfusion: vehicle, AP39 (0...
December 8, 2016: British Journal of Pharmacology
https://www.readbyqxmd.com/read/27924873/cardiac-specific-overexpression-of-mitochondrial-omi-htra2-induces-myocardial-apoptosis-and-cardiac-dysfunction
#2
Ke Wang, Yuexing Yuan, Xin Liu, Wayne Bond Lau, Lin Zuo, Xiaoliang Wang, Lu Ma, Kun Jiao, Jianyu Shang, Wen Wang, Xinliang Ma, Huirong Liu
Myocardial apoptosis is a significant problem underlying ischemic heart disease. We previously reported significantly elevated expression of cytoplasmic Omi/HtrA2, triggers cardiomyocytes apoptosis. However, whether increased Omi/HtrA2 within mitochondria itself influences myocardial survival in vivo is unknown. We aim to observe the effects of mitochondria-specific, not cytoplasmic, Omi/HtrA2 on myocardial apoptosis and cardiac function. Transgenic mice overexpressing cardiac-specific mitochondrial Omi/HtrA2 were generated and they had increased myocardial apoptosis, decreased systolic and diastolic function, and decreased left ventricular remodeling...
December 7, 2016: Scientific Reports
https://www.readbyqxmd.com/read/27915162/high-fat-diet-induces-metabolic-changes-and-reduces-oxidative-stress-in-female-mouse-hearts
#3
Ignasi Barba, Elisabet Miró-Casas, José L Torrecilla, Eulàlia Pladevall, Sergi Tejedor, Rubén Sebastián-Pérez, Marisol Ruiz-Meana, José R Berrendero, Antonio Cuevas, David García-Dorado
After an acute myocardial infarction, obese patients generally have a better prognosis than their leaner counterparts, known as the "obesity paradox". In addition, female sex is associated with a lower risk of cardiac ischemic events and smaller infarct size compared to males. The objective of the present work was to study the metabolic phenotype and mitochondrial function associated to female sex and short-term high-fat diet. (1)H NMR spectra of mice heart extracts were analysed by mRMR variable selection and linear discriminant analysis was used to evaluate metabolic changes...
November 15, 2016: Journal of Nutritional Biochemistry
https://www.readbyqxmd.com/read/27904687/high-fructose-causes-cardiac-hypertrophy-via-mitochondrial-signaling-pathway
#4
Yan-Bo Zhang, Yan-Hai Meng, Shuo Chang, Rong-Yuan Zhang, Chen Shi
High fructose diet can cause cardiac hypertrophy and oxidative stress is a key mediator for myocardial hypertrophy. Disruption of cystic fibrosis transmembrane conductance regulator (CFTR) leads to oxidative stress. This study aims to reveal mitochondrial oxidative stress-related signaling pathway in high fructose-induced cardiac hypertrophy. Mice were fed high fructose to develop cardiac hypertrophy. Fructose and H2O2 were used to induce cardiomyocyte hypertrophy in vitro. Mitochondria-targeted antioxidant SkQ1 was applied to investigate the possible role of mitochondrial reactive oxygen species (ROS)...
2016: American Journal of Translational Research
https://www.readbyqxmd.com/read/27874067/5-htr3-and-5-htr4-located-on-the-mitochondrial-membrane-and-functionally-regulated-mitochondrial-functions
#5
Qingyi Wang, Huiyuan Zhang, Hao Xu, Dongqing Guo, Hui Shi, Yuan Li, Weiwei Zhang, Yuchun Gu
5-HT has been reported to possess significant effects on cardiac activities, but activation of 5-HTR on the cell membrane failed to illustrate the controversial cardiac reaction. Because 5-HT constantly comes across the cell membrane via 5-HT transporter (5-HTT) into the cytoplasm, whether 5-HTR is functional present on the cellular organelles is unknown. Here we show 5-HTR3 and 5-HTR4 were located in cardiac mitochondria, and regulated mitochondrial activities and cellular functions. Knock down 5-HTR3 and 5-HTR4 in neonatal cardiomyocytes resulted in significant increase of cell damage in response to hypoxia, and also led to alternation in heart beating...
November 22, 2016: Scientific Reports
https://www.readbyqxmd.com/read/27872198/in-female-rat-heart-mitochondria-oophorectomy-results-in-loss-of-oxidative-phosphorylation
#6
Natalia Pavón, Alfredo Cabrera-Orefice, Juan Carlos Gallardo-Pérez, Cristina Uribe-Alvarez, Nadia A Rivero-Segura, Edgar Ricardo Vazquez-Martínez, Marco Cerbón, Eduardo Martínez-Abundis, Juan Carlos Torres-Narvaez, Raúl Martínez-Memije, Francisco-Javier Roldán-Gómez, Salvador Uribe-Carvajal
Oophorectomy in adult rats affected cardiac mitochondrial function. Progression of mitochondrial alterations was assessed at one, two and three months after surgery: at one month, very slight changes were observed, which increased at two and three months. Gradual effects included decrease in the rates of oxygen consumption and in respiratory uncoupling in the presence of complex I substrates, as well as compromised Ca(2+) buffering ability. Malondialdehyde concentration increased, whereas the ROS-detoxifying enzyme Mn(2+) superoxide dismutase (MnSOD) and aconitase lost activity...
February 2017: Journal of Endocrinology
https://www.readbyqxmd.com/read/27867086/diazoxide-prevents-reactive-oxygen-species-and-mitochondrial-damage-leading-to-anti-hypertrophic-effects
#7
Aline M Lucas, Francisco R Caldas, Amanda P da Silva, Maximiano M Ventura, Iago M Leite, Ana B Filgueiras, Claúdio G L Silva, Alicia J Kowaltowski, Heberty T Facundo
Pathological cardiac hypertrophy is characterized by wall thickening or chamber enlargement of the heart in response to pressure or volume overload, respectively. This condition will, initially, improve the organ contractile function, but if sustained will render dysfunctional mitochondria and oxidative stress. Mitochondrial ATP-sensitive K(+) channels (mitoKATP) modulate the redox status of the cell and protect against several cardiac insults. Here, we tested the hypothesis that mitoKATP opening (using diazoxide) will avoid isoproterenol-induced cardiac hypertrophy in vivo by decreasing reactive oxygen species (ROS) production and mitochondrial Ca(2+)-induced swelling...
November 17, 2016: Chemico-biological Interactions
https://www.readbyqxmd.com/read/27865838/helix-b-surface-peptide-attenuates-diabetic-cardiomyopathy-via-ampk-dependent-autophagy
#8
Chen Lin, Mingming Zhang, Yingmei Zhang, Kejian Yang, Jianqiang Hu, Rui Si, Guoyong Zhang, Beilei Gao, Xiang Li, Chennian Xu, Congye Li, Qimeng Hao, Wenyi Guo
BACKGROUND: Erythropoietin (EPO) has been reported to exert protective effects on a host of damaged tissues. However, the erythropoietic effect of this hormone can result in high risks of thrombosis, stroke, and hypertension, remarkably limiting the clinical use of EPO. Helix B surface peptide (HBSP) is a small peptide derived from the helix-B domain of EPO. Surprisingly, HBSP retains the tissue protective properties of EPO without altering the hematocrit. Thus, we evaluated the possible role of HBSP on diabetic cardiomyopathy...
November 16, 2016: Biochemical and Biophysical Research Communications
https://www.readbyqxmd.com/read/27859413/zak%C3%AE-antagonizes-and-ameliorates-the-cardiac-hypertrophic-and-apoptotic-effects-induced-by-zak%C3%AE
#9
Chien-Yao Fu, Wei-Wen Kuo, Tsung-Jung Ho, Su-Ying Wen, Ling-Chun Lin, Yan-Shen Tseng, Hui-Chuan Hung, Vijaya Padma Viswanadha, Jaw-Ji Yang, Chih-Yang Huang
ZAK (sterile alpha motif and leucine zipper containing kinase AZK), a serine/threonine kinase with multiple biochemical functions, has been associated with various cell processes, including cell proliferation, cell differentiation, and cardiac hypertrophy. In our previous reports, we found that the activation of ZAKα signaling was critical for cardiac hypertrophy. In this study, we show that the expression of ZAKα activated apoptosis through both a FAS-dependent pathway and a mitochondria-dependent pathway by subsequently inducing caspase-3...
November 16, 2016: Cell Biochemistry and Function
https://www.readbyqxmd.com/read/27832997/effects-of-doxorubicin-on-cardiac-muscle-subsarcolemmal-and-intermyofibrillar-mitochondria
#10
Andreas N Kavazis, Aaron B Morton, Stephanie E Hall, Ashley J Smuder
Doxorubicin (DOX) is a highly effective chemotherapeutic used in the treatment of a broad spectrum of malignancies. However, clinical use of DOX is highly limited by cumulative and irreversible cardiomyopathy that occurs following DOX treatment. The pathogenesis of DOX-induced cardiac muscle dysfunction is complex. However, it has been proposed that the etiology of this myopathy is related to mitochondrial dysfunction, as a result of the dose-dependent increase in the mitochondrial accumulation of DOX. In this regard, cardiac muscle possesses two morphologically distinct populations of mitochondria...
November 8, 2016: Mitochondrion
https://www.readbyqxmd.com/read/27832938/keto-acid-metabolites-of-branched-chain-amino-acids-inhibit-oxidative-stress-induced-necrosis-and-attenuate-myocardial-ischemia-reperfusion-injury
#11
Weibing Dong, Meiyi Zhou, Mei Dong, Bangfen Pan, Yunxia Liu, Jing Shao, Xiaoping Gu, Ying Huang, Guangping Li, Yibin Wang, Haipeng Sun
Branched chain α-keto acids (BCKAs) are endogenous metabolites of branched-chain amino acids (BCAAs). BCAA and BCKA are significantly elevated in pathologically stressed heart and contribute to chronic pathological remodeling and dysfunction. However, their direct impact on acute cardiac injury is unknown. Here, we demonstrated that elevated BCKAs significantly attenuated ischemia-reperfusion (I/R) injury and preserved post I/R function in isolated mouse hearts. BCKAs protected cardiomyocytes from oxidative stress-induced cell death in vitro...
November 8, 2016: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/27818197/lenti-sirna-hsp60-promote-bax-in-mitochondria-and-induces-apoptosis-during-heat-stress
#12
Erbao Song, Shu Tang, Jiao Xu, Bin Yin, Endong Bao, Joerg Hartung
Hsp60 is a typical mitochondrial protein in eukaryotes, and is involved in facilitating the correction of misfolded protein back into the correct conformation. Previous, we identified aspirin-induced HSPs in response to heat stress [1]. To investigate whether Hsp60 can protect against death under heat stress, we used lenti-siRNA to knock down the expression of Hsp60. When exposed to heat stress, more apoptosis was observed with increasing exposure to heat stress, while necrosis was not affected. Furthermore, heat stress induced the loss of mitochondrial membrane potential (ΔΨm) and a significant increase of reactive oxygen species (ROS) produced in mitochondria as measured by TMRE and MitoSOXTM red...
December 2, 2016: Biochemical and Biophysical Research Communications
https://www.readbyqxmd.com/read/27815651/skeletal-muscle-bioenergetics-in-aging-and-heart-failure
#13
Sophia Z Liu, David J Marcinek
Changes in mitochondrial capacity and quality play a critical role in skeletal and cardiac muscle dysfunction. In vivo measurements of mitochondrial capacity provide a clear link between physical activity and mitochondrial function in aging and heart failure, although the cause and effect relationship remains unclear. Age-related decline in mitochondrial quality leads to mitochondrial defects that affect redox, calcium, and energy-sensitive signaling by altering the cellular environment that can result in skeletal muscle dysfunction independent of reduced mitochondrial capacity...
November 5, 2016: Heart Failure Reviews
https://www.readbyqxmd.com/read/27800610/lipocalin-2-ngal-attenuates-autophagy-to-exacerbate-cardiac-apoptosis-induced-by-myocardial-ischemia
#14
Hye Kyoung Sung, Yee Kwan Chan, Meng Han, James Won Suk Jahng, Erfei Song, Danielson Eric, Thorsten Berger, Tak W Mak, Gary Sweeney
Lipocalin-2 (Lcn2; also termed neutrophil gelatinase-associated lipocalin (NGAL)) levels correlate positively with heart failure (HF) yet mechanisms via which Lcn2 contributes to the pathogenesis of HF remian unclear. In this study we used coronary artery ligation surgery to induce ischemia in wild type (wt) mice and this induced a significant increase in myocardial Lcn2. We then compared wt and Lcn2 knockout (KO) mice and observed that wt mice showed greater ischemia-induced caspase-3 activation and DNA damage measured by TUNEL than Lcn2KO mice...
November 1, 2016: Journal of Cellular Physiology
https://www.readbyqxmd.com/read/27799391/exercise-ageing-and-the-lung
#15
Michael A Roman, Harry B Rossiter, Richard Casaburi
This review provides a pulmonary-focused description of the age-associated changes in the integrative physiology of exercise, including how declining lung function plays a role in promoting multimorbidity in the elderly through limitation of physical function. We outline the ageing of physiological systems supporting endurance activity: 1) coupling of muscle metabolism to mechanical power output; 2) gas transport between muscle capillary and mitochondria; 3) matching of muscle blood flow to its requirement; 4) oxygen and carbon dioxide carrying capacity of the blood; 5) cardiac output; 6) pulmonary vascular function; 7) pulmonary oxygen transport; 8) control of ventilation; and 9) pulmonary mechanics and respiratory muscle function...
November 2016: European Respiratory Journal: Official Journal of the European Society for Clinical Respiratory Physiology
https://www.readbyqxmd.com/read/27794519/a-novel-fission-independent-role-of-dynamin-related-protein-1-in-cardiac-mitochondrial-respiration
#16
Huiliang Zhang, Pei Wang, Sara Bisetto, Yisang Yoon, Quan Chen, Shey-Shing Sheu, Wang Wang
AIMS: Mitochondria in adult cardiomyocytes exhibit static morphology and infrequent dynamic changes, despite the high abundance of fission and fusion regulatory proteins in the heart. Previous reports have indicated that fusion proteins may bear functions beyond morphology regulation. Here, we investigated the role of fission protein, dynamin-related protein 1 (DRP1), on mitochondrial respiration regulation in adult cardiomyocytes. METHODS AND RESULTS: By using genetic or pharmacological approaches, we manipulated the activity or protein level of fission and fusion proteins and found they mildly influenced mitochondrial morphology in adult rodent cardiomyocytes, which is in contrast to their significant effect in H9C2 cardiac myoblasts...
October 29, 2016: Cardiovascular Research
https://www.readbyqxmd.com/read/27768893/mof-acetyl-transferase-regulates-transcription-and-respiration-in-mitochondria
#17
Aindrila Chatterjee, Janine Seyfferth, Jacopo Lucci, Ralf Gilsbach, Sebastian Preissl, Lena Böttinger, Christoph U Mårtensson, Amol Panhale, Thomas Stehle, Oliver Kretz, Abdullah H Sahyoun, Sergiy Avilov, Stefan Eimer, Lutz Hein, Nikolaus Pfanner, Thomas Becker, Asifa Akhtar
A functional crosstalk between epigenetic regulators and metabolic control could provide a mechanism to adapt cellular responses to environmental cues. We report that the well-known nuclear MYST family acetyl transferase MOF and a subset of its non-specific lethal complex partners reside in mitochondria. MOF regulates oxidative phosphorylation by controlling expression of respiratory genes from both nuclear and mtDNA in aerobically respiring cells. MOF binds mtDNA, and this binding is dependent on KANSL3. The mitochondrial pool of MOF, but not a catalytically deficient mutant, rescues respiratory and mtDNA transcriptional defects triggered by the absence of MOF...
October 20, 2016: Cell
https://www.readbyqxmd.com/read/27758146/targeting-mitochondrial-dysfunction-in-the-treatment-of-heart-failure
#18
Hani N Sabbah
Heart failure (HF) has reached epidemic proportions worldwide. Despite the availability of drugs that reduce mortality and afford good symptom relief, HF continues to exact a considerable clinical and economic burden. Current HF therapies elicit benefit by reducing cardiac workload by lowering heart rate and loading conditions, thereby reducing myocardial energy demands. Areas covered: Recent recognition that the failing heart is 'energy deprived' and its primary energy source, the mitochondria, is dysfunctional, has focused attention on mitochondria as a worthy therapeutic target...
December 2016: Expert Review of Cardiovascular Therapy
https://www.readbyqxmd.com/read/27754301/lbos-02-02-telmisartan-reducing-monocyte-mitochondria-respiratory-function-is-associated-with-inhibition-of-transient-receptor-potential-channel-canonical-type-3-channels-in-hypertensive-rats
#19
Daoyan Liu
OBJECTIVE: Increased transient receptor potential canonical type 3 (TRPC3) channels have been observed in essential hypertensive patients and spontaneously hypertensive rats (SHR). Our previous study shows that mitochondrial respiratory dysfunctions of blood mononuclear cells link with cardiac disturbance in patients with early-stage heart failure. Telmisartan has beneficial effect on both hypertension and metabolic syndrome. In the present study we tested the hypothesis that telmisartan administration inhibited mitochondrial respiratory function was associated with decreased TRPC3 function in monocytes from genetic hypertensive rats (SHR)...
September 2016: Journal of Hypertension
https://www.readbyqxmd.com/read/27754251/os-36-02-astragaloside-iv-ameliorated-mitochondrial-oxidative-stress-in-hypertensive-mice-with-cardiomyopathy-by-regulating-mitochondrial-ca2-flux
#20
Qiongying Wang, An Xie, Han Xu, Jing Yu
OBJECTIVE: Abnormal Ca handling is thought to be related with triggered activity and mitochondria participate in Ca homeostasis. We evaluated the contribution of Astragaloside IV (ASI) for mitochondrial ROS and Ca Flux to cardiac function by using DOCA-salt hypertensive mice. DESIGN AND METHOD: We used the deoxycorticosterone acetate (DOCA)-salt mouse model. The ventricular myocytes isolated from mice was utilized for action potentials (APs) recording, potassium and L-type Ca currents...
September 2016: Journal of Hypertension
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