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mitochondria and heart failure

Priscila Y Sato, J Kurt Chuprun, Laurel A Grisanti, Meryl C Woodall, Brett R Brown, Rajika Roy, Christopher J Traynham, Jessica Ibetti, Anna M Lucchese, Ancai Yuan, Konstantinos Drosatos, Doug G Tilley, Erhe Gao, Walter J Koch
Increased abundance of GRK2 [G protein-coupled receptor (GPCR) kinase 2] is associated with poor cardiac function in heart failure patients. In animal models, GRK2 contributes to the pathogenesis of heart failure after ischemia-reperfusion (IR) injury. In addition to its role in down-regulating activated GPCRs, GRK2 also localizes to mitochondria both basally and post-IR injury, where it regulates cellular metabolism. We previously showed that phosphorylation of GRK2 at Ser670 is essential for the translocation of GRK2 to the mitochondria of cardiomyocytes post-IR injury in vitro and that this localization promotes cell death...
December 11, 2018: Science Signaling
Xiaoyan Guo, Xiaoguang Wu, Yan Han, Erhu Tian, Jiangtao Cheng
Investigating the molecular mechanisms of myocardial infarction (MI) and subsequent heart failure have gained considerable attention worldwide. Long noncoding RNA (lncRNA) metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) has been previously demonstrated to regulate the proliferation and metastasis of several tumors. However, little is known about the effects of MALAT1 in MI and in regulating the cell date after MI. In our study, first, it was shown that the expression levels of MALAT1 were increased in the MI samples compared with normal tissues using quantitative reverse-transcription polymerase chain reaction...
December 7, 2018: Journal of Cellular Physiology
Vikas Kumar, T R Santhosh Kumar, C C Kartha
Mitochondrial dysfunction is widely recognized as a major factor for the progression of cardiac failure. Mitochondrial uptake of metabolic substrates and their utilization for ATP synthesis, electron transport chain activity, reactive oxygen species levels, ion homeostasis, mitochondrial biogenesis, and dynamics as well as levels of reactive oxygen species in the mitochondria are key factors which regulate mitochondrial function in the normal heart. Alterations in these functions contribute to adverse outcomes in heart failure...
December 10, 2018: Heart Failure Reviews
Márta Sárközy, Zsuzsanna Z A Kovács, Mónika G Kovács, Renáta Gáspár, Gergő Szűcs, László Dux
Chronic kidney disease (CKD) is a public health problem and a recognized risk factor for cardiovascular diseases (CVD). CKD could amplify the progression of chronic heart failure leading to the development of type 4 cardio-renal syndrome (T4CRS). The severity and persistence of heart failure are strongly associated with mortality risk in T4CRS. CKD is also a catabolic state leading to renal sarcopenia which is characterized by the loss of skeletal muscle strength and physical function. Renal sarcopenia also promotes the development of CVD and increases the mortality in CKD patients...
2018: Frontiers in Physiology
Jie Wu, Zhenhua Zeng, Weijin Zhang, Zhiya Deng, Yahui Wan, Yaoyuan Zhang, Sheng An, Qiaobing Huang, Zhongqing Chen
As a nicotinamide adenine dinucleotide (NAD)+ -dependent protein deacetylase, SIRT3 is highly expressed in tissues with high metabolic turnover and mitochondrial content. It has been demonstrated that SIRT3 plays a critical role in maintaining normal mitochondrial biological function through reversible protein lysine deacetylation. SIRT3 has a variety of substrates that are involved in mitochondrial biological processes such as energy metabolism, reactive oxygen species (ROS) production and clearance, electron transport chain (ETC) flux, mitochondrial membrane potential maintenance and mitochondrial dynamics...
November 20, 2018: Free Radical Research
Bin Zhang, Jingyi Zhang, Chenyang Zhang, Xuelian Zhang, Jingxue Ye, Shihuan Kuang, Guibo Sun, Xiaobo Sun
Diabetic cardiomyopathy (DCM) leads to heart failure and death in diabetic patients, no effective treatment is available. Notoginsenoside R1 (NGR1) is a novel saponin that is derived from Panax notoginseng and our previous studies have showed cardioprotective and neuroprotective effects of NGR1. However, its role in protecting against DCM remains unexplored. Herein, we examine potential effects of NGR1 on cardiac function of diabetic db/db mice and H9c2 cardiomyocytes treated by advanced glycation end products (AGEs)...
2018: Frontiers in Pharmacology
Akiyuki Nishimura, Tsukasa Shimauchi, Tomohiro Tanaka, Kakeru Shimoda, Takashi Toyama, Naoyuki Kitajima, Tatsuya Ishikawa, Naoya Shindo, Takuro Numaga-Tomita, Satoshi Yasuda, Yoji Sato, Koichiro Kuwahara, Yoshito Kumagai, Takaaki Akaike, Tomomi Ide, Akio Ojida, Yasuo Mori, Motohiro Nishida
Defective mitochondrial dynamics through aberrant interactions between mitochondria and actin cytoskeleton is increasingly recognized as a key determinant of cardiac fragility after myocardial infarction (MI). Dynamin-related protein 1 (Drp1), a mitochondrial fission-accelerating factor, is activated locally at the fission site through interactions with actin. Here, we report that the actin-binding protein filamin A acted as a guanine nucleotide exchange factor for Drp1 and mediated mitochondrial fission-associated myocardial senescence in mice after MI...
November 13, 2018: Science Signaling
Farzaneh G Tahrir, Dianne Langford, Shohreh Amini, Taha Mohseni Ahooyi, Kamel Khalili
Mitochondria play an important role in maintaining cardiac homeostasis by supplying the major energy required for cardiac excitation-contraction coupling as well as controlling the key intracellular survival and death pathways. Healthy mitochondria generate ATP molecules through an aerobic process known as oxidative phosphorylation (OXPHOS). Mitochondrial injury during myocardial infarction (MI) impairs OXPHOS and results in the excessive production of reactive oxygen species (ROS), bioenergetic insufficiency, and contributes to the development of cardiovascular diseases...
November 11, 2018: Journal of Cellular Physiology
Roberta Coluccia, Salvatore Raffa, Danilo Ranieri, Andrea Micaloni, Sabatino Valente, Gerardo Salerno, Cristina Scrofani, Marco Testa, Giovanna Gallo, Erika Pagannone, Maria Rosaria Torrisi, Massimo Volpe, Speranza Rubattu
Oxidative stress is currently viewed as a key factor in the genesis and progression of Heart Failure (HF). The aim of this study was to characterize the mitochondrial changes linked to oxidative stress generation in circulating peripheral blood mononuclear cells isolated from chronic HF patients (HF_PBMCs) in order to highlight the involvement of mitochondrial dysfunction in the pathophysiology of HF. To assess the production of reactive oxygen species (ROS), mitochondrial function and ultrastructure and the mitophagic flux in circulating PBMCs we enrolled 15 patients with HF and a control group of ten healthy subjects...
October 12, 2018: Oncotarget
Zhiling Qiu, Yuanhui Hu, Yanting Geng, Huaqin Wu, Rongqiang Bo, Jingjing Shi, Jiuchong Wang, Huan Wang
Heart failure caused by myocardial infarction is a common cardiovascular disease with high mortality rate. Myocardial mitophagy is involved in the process of occurrence and development of heart failure. In this study, we aimed to investigate the effects of Xin Fu Kang (XFK) oral liquid on myocardial mitophagy in a rat model of advanced heart failure. The rat model of advanced heart failure was established by ligating the left anterior descending (LAD) artery for eight weeks. Captopril and XFK were given by gavage separately...
2018: American Journal of Translational Research
Dong Seok Lee, Yong Wook Jung
BACKGROUND AND OBJECTIVES: Mitochondria play a key role in the pathophysiology of heart failure and mitochondrial permeability transition pore (MPTP) play a critical role in cell death and a critical target for cardioprotection. The aim of this study was to evaluate the protective effects of cyclosporine A (CsA), one of MPTP blockers, and morphological changes of mitochondria and MPTP related proteins in monocrotaline (MCT) induced pulmonary arterial hypertension (PAH). METHODS: Eight weeks old Sprague-Dawley rats were randomized to control, MCT (60 mg/kg) and MCT plus CsA (10 mg/kg/day) treatment groups...
December 2018: Korean Circulation Journal
E A Ostrakhovitch, S Tabibzadeh
There are numerous theories of aging, a process which still seems inevitable. Aging leads to cancer and multi-systemic disorders as well as chronic diseases including those that impair the functions of endothelial cells, kidney and lung. Decline in age- associated cellular functions leads to neurodegeneration and cognitive decline that affect the quality of life. Accumulation of damage, mutations, metabolic changes, failure in cellular energy production and clearance of altered proteins over the lifetime, and hyperhomocysteinemia, ultimately result in tissue degeneration...
November 1, 2018: Ageing Research Reviews
Kamila Moskowitzova, Borami Shin, Kaifeng Liu, Giovanna Ramirez-Barbieri, Alvise Guariento, David Blitzer, Jerusha K Thedsanamoorthy, Rouan Yao, Erin R Snay, James A H Inkster, Arzoo Orfany, David Zurakowski, Douglas B Cowan, Alan B Packard, Gary A Visner, Pedro J Del Nido, James D McCully
BACKGROUND: Cold ischemia time (CIT) causes ischemia‒reperfusion injury to the mitochondria and detrimentally effects myocardial function and tissue viability. Mitochondrial transplantation replaces damaged mitochondria and enhances myocardial function and tissue viability. Herein we investigated the efficacy of mitochondrial transplantation in enhancing graft function and viability after prolonged CIT. METHODS: Heterotopic heart transplantation was performed in C57BL/6J mice...
September 28, 2018: Journal of Heart and Lung Transplantation
Hazel H Szeto
Mitochondria are the primary source of energy in most tissues and are particularly important for tissues with high energy demand such as skeletal muscle, heart, brain and retina. Mitochondrial dysfunction results in cellular energy deficiency, triggers the production of reactive oxygen species, and initiates various cell death and inflammatory pathways. This review describes a family of mitochondria-targeted tetrapeptides (SS peptides) that have been shown to improve mitochondrial bioenergetics, reduce mitochondrial oxidative stress, and prevent cell death and inflammation...
October 31, 2018: Protein and Peptide Letters
George H Kunkel, Christopher J Kunkel, Hazel Ozuna, Irina Miralda, Suresh C Tyagi
Heart failure (HF) is a functional lack of myocardial performance due to a loss of molecular control over increases in calcium and ROS, resulting in proteolytic degradative advances and cardiac remodeling. Mitochondria are the molecular powerhouse of cells, shifting the sphere of cardiomyocyte stability and performance. Functional mitochondria rely on the molecular abilities of safety factors such as TFAM to maintain physiological parameters. Mitochondrial transcription factor A (TFAM) creates a mitochondrial nucleoid structure around mtDNA, protecting it from mutation, inhibiting NFAT (ROS activator/hypertrophic stimulator), and transcriptionally activates Serca2a to decrease calcium mishandling...
October 23, 2018: Molecular and Cellular Biochemistry
Xurde M Caravia, Víctor Fanjul, Eduardo Oliver, David Roiz-Valle, Alba Morán-Álvarez, Gabriela Desdín-Micó, María Mittelbrunn, Roberto Cabo, José A Vega, Francisco Rodríguez, Antonio Fueyo, Mónica Gómez, Manuel Lobo-González, Héctor Bueno, Gloria Velasco, José M P Freije, Vicente Andrés, Borja Ibáñez, Alejandro P Ugalde, Carlos López-Otín
Different microRNAs (miRNAs), including miR-29 family, may play a role in the development of heart failure (HF), but the underlying molecular mechanisms in HF pathogenesis remain unclear. We aimed at characterizing mice deficient in miR-29 in order to address the functional relevance of this family of miRNAs in the cardiovascular system and its contribution to heart disease. In this work, we show that mice deficient in miR-29a/b1 develop vascular remodeling and systemic hypertension, as well as HF with preserved ejection fraction (HFpEF) characterized by myocardial fibrosis, diastolic dysfunction, and pulmonary congestion, and die prematurely...
October 2018: PLoS Biology
Parisa Samangouei, Gustavo E Crespo-Avilan, Hector Cabrera-Fuentes, Sauri Hernández-Reséndiz, Nur Izzah Ismail, Khairunnisa Binte Katwadi, William A Boisvert, Derek J Hausenloy
Acute myocardial infarction (AMI) and the heart failure (HF) that often follows are among the leading causes of death and disability worldwide. As such novel therapies are needed to reduce myocardial infarct (MI) size, and preserve left ventricular (LV) systolic function in order to reduce the propensity for HF following AMI. Mitochondria are dynamic organelles that can undergo morphological changes by two opposing processes, mitochondrial fusion and fission. Changes in mitochondrial morphology and turnover are a vital part of maintaining mitochondrial health, DNA stability, energy production, calcium homeostasis, cellular division, and differentiation, and disturbances in the balance of fusion and fission can predispose to mitochondrial dysfunction and cell death...
August 2018: Conditioning medicine
Arpita Chowdhury, Abhishek Aich, Gaurav Jain, Katharina Wozny, Christian Lüchtenborg, Magnus Hartmann, Olaf Bernhard, Martina Balleiniger, Ezzaldin Ahmed Alfar, Anke Zieseniss, Karl Toischer, Kaomei Guan, Silvio O Rizzoli, Britta Brügger, Andrè Fischer, Dörthe M Katschinski, Peter Rehling, Jan Dudek
Mitochondria fulfill vital metabolic functions and act as crucial cellular signaling hubs, integrating their metabolic status into the cellular context. Here, we show that defective cardiolipin remodeling, upon loss of the cardiolipin acyl transferase tafazzin, decreases HIF-1α signaling in hypoxia. Tafazzin deficiency does not affect posttranslational HIF-1α regulation but rather HIF-1α gene expression, a dysfunction recapitulated in iPSC-derived cardiomyocytes from Barth syndrome patients with tafazzin deficiency...
October 16, 2018: Cell Reports
Christoph Maack, Thomas Eschenhagen, Nazha Hamdani, Frank R Heinzel, Alexander R Lyon, Dietmar J Manstein, Joseph Metzger, Zoltán Papp, Carlo G Tocchetti, M Birhan Yilmaz, Stefan D Anker, Jean-Luc Balligand, Johann Bauersachs, Dirk Brutsaert, Lucie Carrier, Stefan Chlopicki, John G Cleland, Rudolf A de Boer, Alexander Dietl, Rodolphe Fischmeister, Veli-Pekka Harjola, Stephane Heymans, Denise Hilfiker-Kleiner, Johannes Holzmeister, Gilles de Keulenaer, Giuseppe Limongelli, Wolfgang A Linke, Lars H Lund, Josep Masip, Marco Metra, Christian Mueller, Burkert Pieske, Piotr Ponikowski, Arsen Ristic, Frank Ruschitzka, Petar M Seferovic, Hadi Skouri, Wolfram H Zimmermann, Alexandre Mebazaa
Acute heart failure (HF) and in particular, cardiogenic shock are associated with high morbidity and mortality. A therapeutic dilemma is that the use of positive inotropic agents, such as catecholamines or phosphodiesterase-inhibitors, is associated with increased mortality. Newer drugs, such as levosimendan or omecamtiv mecarbil, target sarcomeres to improve systolic function putatively without elevating intracellular Ca2+. Although meta-analyses of smaller trials suggested that levosimendan is associated with a better outcome than dobutamine, larger comparative trials failed to confirm this observation...
October 8, 2018: European Heart Journal
Cicera Edna Barbosa David, Aline Maria Brito Lucas, Maria Thalyne Silva Araújo, Beatriz Neves Coelho, Juarez Braga Soares Neto, Bruna Raysa Campos Portela, Anna Lídia Nunes Varela, Alicia J Kowaltowski, Heberty T Facundo
Oxidative stress has been implicated in the pathogenesis of cardiac hypertrophy and associated heart failure. Cardiac tissue grows in response to pressure or volume overload, leading to wall thickening or chamber enlargement. If sustained, this condition will lead to a dysfunctional cardiac tissue and oxidative stress. Calorie restriction (CR) is a powerful intervention to improve health and delay aging. Here, we investigated whether calorie restriction in mice prevented isoproterenol-induced cardiac hypertrophy in vivo by avoiding reactive oxygen species (ROS) production and maintaining antioxidant enzymatic activity...
September 5, 2018: Journal of Nutritional Biochemistry
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