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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
#1
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/28070695/barth-syndrome-connecting-cardiolipin-to-cardiomyopathy
#2
REVIEW
Nikita Ikon, Robert O Ryan
The Barth syndrome (BTHS) is caused by an inborn error of metabolism that manifests characteristic phenotypic features including altered mitochondrial membrane phospholipids, lactic acidosis, organic acid-uria, skeletal muscle weakness and cardiomyopathy. The underlying cause of BTHS has been definitively traced to mutations in the tafazzin (TAZ) gene locus on chromosome X. TAZ encodes a phospholipid transacylase that promotes cardiolipin acyl chain remodeling. Absence of tafazzin activity results in cardiolipin molecular species heterogeneity, increased levels of monolysocardiolipin and lower cardiolipin abundance...
January 9, 2017: Lipids
https://www.readbyqxmd.com/read/28069019/ppars-modulate-cardiac-metabolism-and-mitochondrial-function-in-diabetes
#3
REVIEW
Ting-Wei Lee, Kuan-Jen Bai, Ting-I Lee, Tze-Fan Chao, Yu-Hsun Kao, Yi-Jen Chen
Diabetic cardiomyopathy is a major complication of diabetes mellitus (DM). Currently, effective treatments for diabetic cardiomyopathy are limited. The pathophysiology of diabetic cardiomyopathy is complex, whereas mitochondrial dysfunction plays a vital role in the genesis of diabetic cardiomyopathy. Metabolic regulation targeting mitochondrial dysfunction is expected to be a reasonable strategy for treating diabetic cardiomyopathy. Peroxisome proliferator-activated receptors (PPARs) are master executors in regulating glucose and lipid homeostasis and also modulate mitochondrial function...
January 10, 2017: Journal of Biomedical Science
https://www.readbyqxmd.com/read/28051329/regulation-of-the-cardioprotective-adiponectin-and-its-receptor-adipor1-by-salt
#4
Nicholas Arnold, Abuzar Mahmood, Maya Ramdas, Paul P Ehlinger, Lakshmi Pulakat
Both circulating adiponectin (APN) and cardiac APN exert cardioprotective effects and improve insulin sensitivity and mitochondrial function. Low circulating APN serves as a biomarker for cardiovascular risk. Ablation of adiponectin receptor 1 (AdipoR1) causes myocardial mitochondrial dysfunction. Although high salt intake is a contributor to cardiovascular disease, how it modulates the expression of APN or AdipoR1 in cardiomyocytes is not known. We report that APN mRNA expression was attenuated in a dose-dependent manner in mouse cardiomyocyte cell line HL-1 exposed to salt concentrations ranging from 0...
November 30, 2016: Canadian Journal of Physiology and Pharmacology
https://www.readbyqxmd.com/read/28051130/the-histone-3-lysine-9-methyltransferase-inhibitor-chaetocin-improves-prognosis-in-a-rat-model-of-high-salt-diet-induced-heart-failure
#5
Tomohiko Ono, Naomi Kamimura, Tomohiro Matsuhashi, Toshihiro Nagai, Takahiko Nishiyama, Jin Endo, Takako Hishiki, Tsuyoshi Nakanishi, Noriaki Shimizu, Hirotoshi Tanaka, Shigeo Ohta, Makoto Suematsu, Masaki Ieda, Motoaki Sano, Keiichi Fukuda, Ruri Kaneda
Histone acetylation has been linked to cardiac hypertrophy and heart failure. However, the pathological implications of changes in histone methylation and the effects of interventions with histone methyltransferase inhibitors for heart failure have not been fully clarified. Here, we focused on H3K9me3 status in the heart and investigated the effects of the histone H3K9 methyltransferase inhibitor chaetocin on prognoses in Dahl salt-sensitive rats, an animal model of chronic heart failure. Chaetocin prolonged survival and restored mitochondrial dysfunction...
January 4, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28034298/effective-agents-targeting-the-mitochondria-and-apoptosis-to-protect-the-heart
#6
Eltyeb Abdelwahid, Aurimas Stulpinas, Audrone Kalvelyte
A wide variety of agents have been traditionally used in cardiovascular medicine worldwide and their precise mechanisms of action have been demonstrated to be largely related to the cardiomyocyte mitochondria and apoptosis. Abnormalities in the structure and function of the mitochondria and mutations in mitochondrial DNA can decrease energy production, alter the redox system, impair calcium homeostasis, and induce the mitochondrial permeability transition pore (MPTP), causing cell death. All of these data provide evidence of mitochondrial signaling pathways as targets to downregulate cardiac cell apoptosis and thus to prevent and treat cardiovascular diseases...
December 29, 2016: Current Pharmaceutical Design
https://www.readbyqxmd.com/read/28008641/effects-of-mirnas-on-myocardial-apoptosis-by-modulating-mitochondria-related-proteins
#7
REVIEW
Yanfang Zhao, Murugavel Ponnusamy, Yanhan Dong, Lei Zhang, Kun Wang, Peifeng Li
Myocardial apoptosis play a vital role in pathogenesis of cardiovascular diseases. The intrinsic pathway of apoptosis (mitochondrial apoptosis pathway) and abnormal mitochondrial fission and fusion have a detrimental effect on cells under a variety of intracellular stresses including hypoxia, oxidative stress, drug toxicity or DNA damage and contributes to the development of heart failure (HF), myocardial infarction (MI), diabetic cardiomyopathy and ischemia/reperfusion injury (I/R). MicroRNAs (miRNAs) are endogenous short noncoding RNAs, which target 3'-untranslated region of mRNA to switch off gene expression...
December 23, 2016: Clinical and Experimental Pharmacology & Physiology
https://www.readbyqxmd.com/read/28004807/expert-consensus-document-mitochondrial-function-as-a-therapeutic-target-in-heart-failure
#8
David A Brown, Justin B Perry, Mitchell E Allen, Hani N Sabbah, Brian L Stauffer, Saame Raza Shaikh, John G F Cleland, Wilson S Colucci, Javed Butler, Adriaan A Voors, Stefan D Anker, Bertram Pitt, Burkert Pieske, Gerasimos Filippatos, Stephen J Greene, Mihai Gheorghiade
Heart failure is a pressing worldwide public-health problem with millions of patients having worsening heart failure. Despite all the available therapies, the condition carries a very poor prognosis. Existing therapies provide symptomatic and clinical benefit, but do not fully address molecular abnormalities that occur in cardiomyocytes. This shortcoming is particularly important given that most patients with heart failure have viable dysfunctional myocardium, in which an improvement or normalization of function might be possible...
December 22, 2016: Nature Reviews. Cardiology
https://www.readbyqxmd.com/read/27998959/exogenous-h2s-regulates-endoplasmic-reticulum-mitochondria-cross-talk-to-inhibit-apoptotic-pathways-in-stz-induced-type-i-diabetes
#9
Fan Yang, Xiangjing Yu, Ting Li, Jianjun Wu, YaJun Zhao, Aili Sun, Shiyun Dong, Jichao Wu, Xin Zhong, Changqing Xu, Fanghao Lu, Weihua Zhang
BACKGROUND: The upregulation of reactive oxygen species (ROS) is a primary cause of cardiomyocyte apoptosis in Diabetes cardiomyopathy (DCM). Mitofusin-2 (Mfn-2) is a key protein that bridges the mitochondria and endoplasmic reticulum(ER). Hydrogen sulfide (H2S)-mediated cardioprotection is related to antioxidant effects. The present study demonstrated that H2S inhibited the interaction between the ER and mitochondrial apoptotic pathway. METHODS: This study investigated cardiac function, ultrastructural changes in the ER and mitochondria, apoptotic rate using TUNEL and the expression of ER stress-associated proteins and mitochondrial apoptotic proteins in cardiac tissues in STZ-induced type I diabetic rats treated with or without NaHS (donor of H2S)...
December 20, 2016: American Journal of Physiology. Endocrinology and Metabolism
https://www.readbyqxmd.com/read/27998213/mitochondrial-omi-htra2-promotes-caspase-activation-through-cleavage-of-hax-1-in-aging-heart
#10
Xin Liu, Jinghui Lei, Ke Wang, Lu Ma, Dan Liu, Yunhui Du, Ye Wu, Suli Zhang, Wen Wang, Xin L Ma, Huirong Liu
Mitochondrial homeostasis is a key process involved in cellular destiny and organic function. When mitochondrial status is abnormal, it will become a "death motor". Impaired mitochondria lead to the release of cytochrome c, and then trigger mitochondria-induced caspase activation. Omi/HtrA2, a serine protease, locates in mitochondria, and involves in mitochondrial homeostasis. Increased Omi/HtrA2 is observed in aging cardiac tissues, and whether this has effects on mitochondrial status hasn't been reported...
December 21, 2016: Rejuvenation Research
https://www.readbyqxmd.com/read/27991671/the-mitochondrial-calcium-uniporter-in-the-heart-energetics-and-beyond
#11
Jennifer Q Kwong
Ca(2+) and mitochondria are inextricably linked to cardiac function and dysfunction. Ca(2+) is central cardiac excitation-contraction coupling and stimulates mitochondrial energy production to fuel contraction. Under pathological conditions of dysregulated Ca(2+) cycling, mitochondrial Ca(2+) overload activates cellular death pathways. Thus, in the cardiomyocyte, the mitochondrial Ca(2+) microdomain is where contraction, energy and death collide. A key component of mitochondrial Ca(2+) signalling is the mitochondrial Ca(2+) uniporter (MCU) complex (uniplex), an inner membrane Ca(2+) transporter and major pathway of mitochondrial Ca(2+) entry...
December 19, 2016: Journal of Physiology
https://www.readbyqxmd.com/read/27938904/myocardial-rescue-with-autologous-mitochondrial-transplantation-in-a-porcine-model-of-ischemia-reperfusion
#12
Aditya K Kaza, Isaac Wamala, Ingeborg Friehs, Joseph D Kuebler, Rahul H Rathod, Ignacio Berra, Maria Ericsson, Rouan Yao, Jerusha K Thedsanamoorthy, David Zurakowski, Sidney Levitsky, Pedro J Del Nido, Douglas B Cowan, James D McCully
OBJECTIVE: To demonstrate the clinical efficacy of autologous mitochondrial transplantation in preparation for translation to human application using an in vivo swine model. METHODS: A left mini-thoracotomy was performed on Yorkshire pigs. The pectoralis major was dissected, and skeletal muscle tissue was removed and used for the isolation of autologous mitochondria. The heart was subjected to regional ischemia (RI) by temporarily snaring the circumflex artery...
November 15, 2016: Journal of Thoracic and Cardiovascular Surgery
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
#13
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
#14
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
#15
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
#16
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
#17
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
#18
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
#19
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...
January 5, 2017: Chemico-biological Interactions
https://www.readbyqxmd.com/read/27865838/helix-b-surface-peptide-attenuates-diabetic-cardiomyopathy-via-ampk-dependent-autophagy
#20
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...
January 22, 2017: Biochemical and Biophysical Research Communications
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