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mitochondria and heart failure

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
Rebecca M Parodi-Rullán, Jadira Soto-Prado, Jesús Vega-Lugo, Xavier Chapa-Dubocq, Sara I Díaz-Cordero, Sabzali Javadov
BACKGROUND/AIMS: The mitochondrial permeability transition pore opening plays a critical role in the pathogenesis of myocardial infarction. Inhibition of cyclophilin-D (CyP-D), a key regulator of the mitochondrial permeability transition pore, has been shown to exert cardioprotective effects against ischemia-reperfusion injury on various animal models, mostly in males. However, failure of recent clinical trials requires a detailed elucidation of the cardioprotective efficacy of CyP-D inhibition...
October 3, 2018: Cellular Physiology and Biochemistry
Genzou Takemura, Hiromitsu Kanamori, Hideshi Okada, Akiko Tsujimoto, Nagisa Miyazaki, Shusaku Miyata, Hideaki Ohta, Yoshiaki Kawase, Makoto Ono, Mamoru Mochizuki, Shigeki Kobayashi, Kenji Onoue, Tomoya Nakano, Yasuhiro Sakaguchi, Hitoshi Matsuo, Masafumi Yano, Yoshihiko Saito
During electron microscopic examination of 156 consecutive human endomyocardial biopsy specimens, we found marked mitochondrial deformity within a single cardiomyocyte in each of 4 specimens. The deformed mitochondria were unevenly distributed, but the deformities were confined to the one cardiomyocyte. Those affected cardiomyocytes were accompanied by nonspecific degenerative changes such as nuclear hypertrophy and/or rarefaction of the myofibrils. Mitochondria in all other cells within the specimens appeared normal...
November 2017: Journal of Cardiology Cases
Joon-Chul Kim, Min-Jeong Son, Sun-Hee Woo
Myocardium is subjected to a variety of forces with each contraction, such as stretch, afterload, and shear stress, and adapts to those mechanical stimuli. These mechanical stimuli increase in heart failure, valvular heart disease and hypertension that are clinically associated with arrhythmia and myocyte remodeling. To understand cellular and molecular basis of mechanical stress-mediated cardiac dysfunction and remodeling, several experimental approaches have been successfully used in single cardiac myocytes...
September 29, 2018: Archives of Biochemistry and Biophysics
Sheila Moreira da Silva Guimarães, Wanise Maria de Souza Cruz, Guilherme de Souza Weigert, Fernanda Bertão Scalco, Alexandre Siciliano Colafranceschi, Marcia Gonçalves Ribeiro, Gilson Teles Boaventura
The heart has an intense aerobic metabolism and is among the most metabolically active organs in the body. Its tissue stores fatty acid, the main energetic substrate, and requires high concentrations of plasma L-carnitine. This nutrient is essential in the transport of fatty acids to the mitochondria to generate energy and maintain the proper concentration of coenzyme A free. In decompensated chronic heart failure metabolic changes, associated with inflammation, alter the metabolism of L-carnitine and compromise cardiac energy metabolism...
September 26, 2018: Archives of Medical Research
Philippe Hantson
BACKGROUND: Dilated cardiomyopathy is a frequent disease responsible for 40-50% of cases of heart failure. Idiopathic cardiomyopathy is a primary disorder often related to familial/genetic predisposition. Before the diagnosis of idiopathic cardiomyopathy is made, clinicians must not only rule out viral and immune causes, but also toxic causes such as drugs, environmental agents, illicit substances and natural toxins. OBJECTIVE: The objective of this review is to present recent data on the mechanisms underlying toxic cardiomyopathy...
September 27, 2018: Clinical Toxicology
Atsushi Shibata, Yasuo Sugano, Akito Shimouchi, Tetsuro Yokokawa, Naoya Jinno, Hideaki Kanzaki, Keiko Ohta-Ogo, Yoshihiko Ikeda, Hideshi Okada, Takeshi Aiba, Kengo Kusano, Mikiyasu Shirai, Hatsue Ishibashi-Ueda, Satoshi Yasuda, Hisao Ogawa, Toshihisa Anzai
Objective: Hydrogen excretion is thought to be related to systemic antioxidation activity. H2 selectively reduces the hydroxyl radical of free hydrogen (·OH), a highly cytotoxic form of reactive oxygen species, in cultured cells. Methods: We investigated whether exhaled H2 decreased during night sleep, reflected ·OH production and was associated with heart failure severity. We enrolled 108 patients with chronic heart failure (CHF) and 15 control participants without CHF...
2018: Open Heart
Fang Cao, Sevasti Zervou, Craig A Lygate
Restoring blood flow following an acute myocardial infarction saves lives, but results in tissue damage due to ischaemia-reperfusion injury (I/R). Ameliorating this damage is a major research goal to improve recovery and reduce subsequent morbidity due to heart failure. Both the ischaemic and reperfusion phases represent crises of cellular energy provision in which the mitochondria play a central role. This mini-review will explore the rationale and therapeutic potential of augmenting the creatine kinase (CK) energy shuttle, which constitutes the primary short-term energy buffer and transport system in the cardiomyocyte...
September 20, 2018: Biochemical Society Transactions
Guodong Pan, Mandar Deshpande, Haiyan Pang, Suresh Selvaraj Palaniyandi
A vast majority of type-2 diabetic patients (~65%) die of cardiovascular complications including heart failure (HF). In diabetic hearts, levels of 4-hydroxy-2-nonenal (4HNE), a reactive aldehyde that is produced upon lipid peroxidation, were increased. We also demonstrated that in diabetic hearts, there is a decrease in the activity of aldehyde dehydrogenase (ALDH) 2, a primary detoxifying enzyme present in cardiac mitochondria. A single point mutation at E487K of ALDH2 in East Asians known as ALDH2 * 2 intrinsically lowers ALDH2 activity...
September 19, 2018: European Journal of Pharmacology
Dongxia Zhang, Jingtao Ma
BACKGROUND Patients treated with 5-FU can develop rare but potentially severe cardiac effects, including cardiomyopathy, angina pectoris, ventricular tachycardia, heart failure, acute myocardial infarction, and cardiogenic shock. The specific pathologies and mechanisms are not fully understood. Research found that mitochondrial dynamics are widely detected in many angiocardiopathies. Therefore, in the present study we studied the mitochondrial damage and explored the role of mitochondrial fusion/fission proteins on myocardium of rats treated with 5-fluorouracil (5-FU)...
September 21, 2018: Medical Science Monitor: International Medical Journal of Experimental and Clinical Research
Ligia Akemi Kiyuna, Rudá Prestes E Albuquerque, Che-Hong Chen, Daria Mochly-Rosen, Julio Cesar Batista Ferreira
Mitochondrial dysfunction characterized by impaired bioenergetics, oxidative stress and aldehydic load is a hallmark of heart failure. Recently, different research groups have provided evidence that selective activation of mitochondrial detoxifying systems that counteract excessive accumulation of ROS, RNS and reactive aldehydes is sufficient to stop cardiac degeneration upon chronic stress, such as heart failure. Therefore, pharmacological and non-pharmacological approaches targeting mitochondria detoxification may play a critical role in the prevention or treatment of heart failure...
September 15, 2018: Free Radical Biology & Medicine
Hussam M Daghistani, Bodour S Rajab, Ashraf Kitmitto
A hallmark of heart failure is mitochondrial dysfunction leading to a bioenergetics imbalance in the myocardium. Consequently, there is much interest in targeting mitochondrial abnormalities to attenuate the pathogenesis of heart failure. This review discusses i) how electron microscopy (EM) techniques have been fundamental for current understanding of mitochondrial structure-function ii) the paradigm shift in resolutions now achievable by 3-D EM techniques due to the introduction of direct detection devices and phase plate technology, and iii) the application of EM for unravelling mitochondrial pathological remodelling in heart failure...
September 18, 2018: British Journal of Pharmacology
Zheng Cheng, Mingming Zhang, Jianqiang Hu, Jie Lin, Xinyu Feng, Shanjie Wang, Tingting Wang, Erhe Gao, Haichang Wang, Dongdong Sun
AIMS: Angiotension II (Ang II) plays a central role in the pathogenesis of renin-angiotensin-aldosterone system (RAAS)-induced heart failure. Mst1 exerts its function in cardiomyocytes subjected to pathological stimuli via inhibiting autophagy and aggravating apoptosis, but its role in RAAS-mediated cardiac injury is still unknown. Here, we aimed to determine whether cardiomyocyte-specific Mst1 knockout can alleviate Ang II-induced cardiac injury by improving cardiomyocyte autophagy and whether these functions depend on Ang II receptors...
September 4, 2018: Journal of Molecular and Cellular Cardiology
Dan Chen, Xia Li, LiTing Zhang, Mei Zhu, Ling Gao
A high-fat diet (HFD) has been associated with heart failure and arrhythmias; however, the molecular mechanisms underlying these associations are poorly understood. The mitochondria play an essential role in optimal heart performance, most of the energy for which is obtained from the oxidation of fatty acids. As such, chronic exposure to excess fatty acids may cause mitochondrial dysfunction and heart failure. To investigate the effects of a HFD on the mitochondrial function in the myocardium, 40 male rats were randomly divided into two groups and fed with either a normal diet or a HFD for 28 weeks...
September 1, 2018: Journal of Cellular Biochemistry
Masaya Tsuda, Arata Fukushima, Junichi Matsumoto, Shingo Takada, Naoya Kakutani, Hideo Nambu, Katsuma Yamanashi, Takaaki Furihata, Takashi Yokota, Koichi Okita, Shintaro Kinugawa, Toshihisa Anzai
BACKGROUND: Exercise intolerance is a common clinical feature and is linked to poor prognosis in patients with heart failure (HF). Skeletal muscle dysfunction, including impaired energy metabolism in the skeletal muscle, is suspected to play a central role in this intolerance, but the underlying mechanisms remain elusive. Lysine acetylation, a recently identified post-translational modification, has emerged as a major contributor to the derangement of mitochondrial metabolism. We thus investigated whether mitochondrial protein acetylation is associated with impaired skeletal muscle metabolism and lowered exercise capacity in both basic and clinical settings of HF...
August 30, 2018: Journal of Cachexia, Sarcopenia and Muscle
E Dale Abel
Mitochondria are the metabolic powerhouses of cells. In addition to generating adenosine triphosphate (ATP), they play important roles in cell survival pathways such as apoptosis and necrosis. Mitochondrial size and shape are dynamically regulated by a process known as mitochondrial dynamics. The significance of this process in metabolically active cells such as skeletal and cardiac muscle are only now beginning to be elucidated. In cardiac muscle, mitochondrial dynamics plays an important role in mitochondrial quality control and defects in regulatory pathways that govern these processes and leads to heart failure...
2018: Transactions of the American Clinical and Climatological Association
Man Xu, Run-Qing Xue, Yi Lu, Su-Yun Yong, Qing Wu, Yan-Ling Cui, Xiao-Ting Zuo, Xiao-Jiang Yu, Ming Zhao, Wei-Jin Zang
Aim: Cardiac hypertrophy is characterised by a shift in metabolic substrate utilisation, but the molecular events underlying the metabolic remodelling remain poorly understood. We explored metabolic remodelling and mitochondrial dysfunction in cardiac hypertrophy and investigated the cardioprotective effects of choline. Methods and Results: The experiments were conducted using a model of ventricular hypertrophy by partially banding the abdominal aorta of Sprague Dawley rats...
August 27, 2018: Cardiovascular Research
T A Popova, E A Muzyko, M V Kustova, M A Bychenkova, V N Perfilova, I I Prokofiev, M A Samoylova, I N Tyurenkov, G M Latypova, V A Kataev
Experimental chronic heart failure (CHF), caused by administration of L-isoproterenol (2.5 mg/kg twice a day intraperitoneally for 21 days), promotes uncoupling of respiration and oxidative phosphorylation. The rate of mitochondrial oxygen consumption in the metabolic state V3 by Chance in animals with CHF decreased by 53.3% (p<0.05) with malate using (as an oxidation substrate feeding сomplex I of the electron transport chain (ETC)), by 70.6% (p<0.05) with succinate using (сomplex II substrate) and by 63...
August 2018: Biomedit︠s︡inskai︠a︡ Khimii︠a︡
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