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heart failure and autophagy

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https://www.readbyqxmd.com/read/28801076/early-development-of-right-ventricular-ischemic-lesions-in-a-novel-large-animal-model-of-acute-right-heart-failure-in-chronic-thromboembolic-pulmonary-hypertension
#1
David Boulate, Jennifer Arthur Ataam, Andrew J Connolly, Genevieve Giraldeau, Myriam Amsallem, Benoit Decante, Lilia Lamrani, Elie Fadel, Peter Dorfmuller, Frederic Perros, Francois Haddad, Olaf Mercier
BACKGROUND: Our aim was to develop a model of acute right heart failure (ARHF) in the setting of pulmonary hypertension and to characterize acute right ventricular lesions that develop early after hemodynamic restoration. METHODS AND RESULTS: We used a described piglet model of chronic pulmonary hypertension (cPH) induced by pulmonary artery occlusions. We induced ARHF in animals with cPH (ARHF-cPH group, n=9) by volume loading and iterative acute pulmonary embolisms until hemodynamic compromise followed by dobutamine infusion for hemodynamic restoration prior to sacrifice for right ventricular tissue evaluation...
August 8, 2017: Journal of Cardiac Failure
https://www.readbyqxmd.com/read/28794819/upregulation-of-autophagy-genes-and-the-unfolded-protein-response-in-human-heart-failure
#2
Brian C Jensen, Scott J Bultman, Darcy Holley, Wei Tang, Gustaaf de Ridder, Salvatore Pizzo, Dawn Bowles, Monte S Willis
The cellular environment of the mammalian heart constantly is challenged with environmental and intrinsic pathological insults, which affect the proper folding of proteins in heart failure. The effects of damaged or misfolded proteins on the cell can be profound and result in a process termed "proteotoxicity". While proteotoxicity is best known for its role in mediating the pathogenesis of neurodegenerative diseases such as Alzheimer's disease, its role in human heart failure also has been recognized. The UPR involves three branches, including PERK, ATF6, and IRE1...
2017: International Journal of Clinical and Experimental Medicine
https://www.readbyqxmd.com/read/28760737/docetaxel-reverses-pulmonary-vascular-remodeling-by-decreasing-autophagy-and-resolves-right-ventricular-fibrosis
#3
Yasmine F Ibrahim, Nataliia V Shults, Vladyslava Rybka, Yuichiro J Suzuki
Pulmonary arterial hypertension remains a fatal disease despite the availability of approved vasodilators. Since vascular remodeling contributes to increased pulmonary arterial pressure, new agents that reduce the thickness of pulmonary vascular walls have therapeutic potential. Thus, anti-tumor agents that are capable of killing cells were investigated. Testing of various anti-tumor drugs identified that docetaxel is a superior drug for killing proliferating pulmonary artery smooth muscle cells compared with other drugs including gemcitabine, methotrexate and ifosfamide...
July 31, 2017: Journal of Pharmacology and Experimental Therapeutics
https://www.readbyqxmd.com/read/28751931/a-review-of-the-molecular-mechanisms-underlying-the-development-and-progression-of-cardiac-remodeling
#4
REVIEW
Leonardo Schirone, Maurizio Forte, Silvia Palmerio, Derek Yee, Cristina Nocella, Francesco Angelini, Francesca Pagano, Sonia Schiavon, Antonella Bordin, Albino Carrizzo, Carmine Vecchione, Valentina Valenti, Isotta Chimenti, Elena De Falco, Sebastiano Sciarretta, Giacomo Frati
Pathological molecular mechanisms involved in myocardial remodeling contribute to alter the existing structure of the heart, leading to cardiac dysfunction. Among the complex signaling network that characterizes myocardial remodeling, the distinct processes are myocyte loss, cardiac hypertrophy, alteration of extracellular matrix homeostasis, fibrosis, defective autophagy, metabolic abnormalities, and mitochondrial dysfunction. Several pathophysiological stimuli, such as pressure and volume overload, trigger the remodeling cascade, a process that initially confers protection to the heart as a compensatory mechanism...
2017: Oxidative Medicine and Cellular Longevity
https://www.readbyqxmd.com/read/28691995/the-role-of-psychological-stress-on-heart-autophagy-in-mice-with-heart-failure
#5
Xiao-Ting Lu, Xiao-Qiong Liu, Bo Wang, Yuan-Yuan Sun, Rui-Xue Yang, Yi-Fan Xing, Ping Sun, Ying-Bin Wang, Yu-Xia Zhao
OBJECTIVE: Psychological stress in chronic heart failure (CHF) is associated with systemic neurohormonal and immune system responses and increased mortality. Autophagy refers to the biological process of degradation and recycling of dysfunctional cellular components. We investigated the role of psychological stress on autophagy function in CHF mice. RESULTS: A one-week stress exposure significantly increased serum levels of corticosterone and Ang II (P= .000), increased levels of oxidative stress, induced overt heart failure, and increased mortality (P =...
July 7, 2017: Psychosomatic Medicine
https://www.readbyqxmd.com/read/28670364/lipocalin-2-induces-nlrp3-inflammasome-activation-via-hmgb1-induced-tlr4-signaling-in-heart-tissue-of-mice-under-pressure-overload-challenge
#6
Erfei Song, James Ws Jahng, Lisa P Chong, Hye K Sung, Meng Han, Cuiting Luo, Donghai Wu, Stellar Boo, Boris Hinz, Matthew A Cooper, Avril Ab Robertson, Thorsten Berger, Tak W Mak, Isaac George, P Christian Schulze, Yu Wang, Aimin Xu, Gary Sweeney
Lipocalin-2 (also known as NGAL) levels are elevated in obesity and diabetes yet relatively little is known regarding effects on the heart. We induced pressure overload (PO) in mice and found that lipocalin-2 knockout (LKO) mice exhibited less PO-induced autophagy and NLRP3 inflammasome activation than Wt. PO-induced mitochondrial damage was reduced and autophagic flux greater in LKO mice, which correlated with less cardiac dysfunction. All of these observations were negated upon adenoviral-mediated restoration of normal lipocalin-2 levels in LKO...
2017: American Journal of Translational Research
https://www.readbyqxmd.com/read/28667023/autophagy-inflammasome-interplay-in-heart-failure-a-systematic-review-on-basics-pathways-and-therapeutic-perspectives
#7
Bonnie Chiu, Eugeniu Jantuan, Fan Shen, Brian Chiu, Consolato Sergi
Aging of the population contributes to the increasing prevalence of heart failure. Autophagy is an evolutionarily conserved process aiming to degrade both long-lived proteins and damaged or excessive cyto-organelles via the lysosomal-mediated pathway. Although autophagy is involved in the normal homeostasis of cardiovascular cells, upregulation of autophagy and its abnormal modulation by inflammation may lead to cardiovascular functional decline and heart failure. Despite major improvements in the prevention, diagnosis, and treatment of cardiovascular diseases, heart failure remains one of the major diagnostic and therapeutic challenges...
May 2017: Annals of Clinical and Laboratory Science
https://www.readbyqxmd.com/read/28660894/proteostasis-in-cardiac-health-and-disease
#8
REVIEW
Robert H Henning, Bianca J J M Brundel
The incidence and prevalence of cardiac diseases, which are the main cause of death worldwide, are likely to increase because of population ageing. Prevailing theories about the mechanisms of ageing feature the gradual derailment of cellular protein homeostasis (proteostasis) and loss of protein quality control as central factors. In the heart, loss of protein patency, owing to flaws in genetically-determined design or because of environmentally-induced 'wear and tear', can overwhelm protein quality control, thereby triggering derailment of proteostasis and contributing to cardiac ageing...
June 29, 2017: Nature Reviews. Cardiology
https://www.readbyqxmd.com/read/28640445/ubiquitin-ligases-and-posttranslational-regulation-of-energy-in-the-heart-the-hand-that-feeds
#9
David I Brown, Traci L Parry, Monte S Willis
Heart failure (HF) is a costly and deadly syndrome characterized by the reduced capacity of the heart to adequately provide systemic blood flow. Mounting evidence implicates pathological changes in cardiac energy metabolism as a contributing factor in the development of HF. While the main source of fuel in the healthy heart is the oxidation of fatty acids, in the failing heart the less energy efficient glucose and glycogen metabolism are upregulated. The ubiquitin proteasome system plays a key role in regulating metabolism via protein-degradation/regulation of autophagy and regulating metabolism-related transcription and cell signaling processes...
June 18, 2017: Comprehensive Physiology
https://www.readbyqxmd.com/read/28598232/exercise-reestablishes-autophagic-flux-and-mitochondrial-quality-control-in-heart-failure
#10
Juliane C Campos, Bruno B Queliconi, Luiz H M Bozi, Luiz R G Bechara, Paulo M M Dourado, Allen M Andres, Paulo R Jannig, Kátia M S Gomes, Vanessa O Zambelli, Cibele Rocha-Resende, Silvia Guatimosim, Patricia C Brum, Daria Mochly-Rosen, Roberta A Gottlieb, Alicia J Kowaltowski, Julio C B Ferreira
We previously reported that facilitating the clearance of damaged mitochondria through macroautophagy/autophagy protects against acute myocardial infarction. Here we characterized the impact of exercise, a safe strategy against cardiovascular disease, on cardiac autophagy and its contribution to mitochondrial quality control, bioenergetics and oxidative damage in a post-myocardial infarction-induced heart failure animal model. We found that failing hearts displayed reduced autophagic flux depicted by accumulation of autophagy-related markers and loss of responsiveness to chloroquine treatment at 4 and 12 weeks after myocardial infarction...
June 9, 2017: Autophagy
https://www.readbyqxmd.com/read/28590260/ghrelin-and-autophagy
#11
Silvia Ezquerro, Gema Frühbeck, Amaia Rodríguez
PURPOSE OF REVIEW: A compromised autophagy is associated with the onset of obesity, type 2 diabetes, nonalcoholic fatty liver disease, cardiovascular and neurodegenerative diseases. Our aim is to review the potential role of ghrelin, a gut hormone involved in energy homeostasis, in the regulation of autophagy. RECENT FINDINGS: In the recent years, it has been demonstrated that autophagy constitutes an important mechanism by which ghrelin exerts a plethora of central and peripheral actions...
September 2017: Current Opinion in Clinical Nutrition and Metabolic Care
https://www.readbyqxmd.com/read/28576834/autophagy-modulation-a-potential-therapeutic-approach-in-cardiac-hypertrophy
#12
Xuejun Wang, Taixing Cui
Autophagy is an evolutionarily conserved process used by the cell to degrade cytoplasmic contents for quality control, survival for temporal energy crisis, and catabolism and recycling. Rapidly increasing evidence has revealed an important pathogenic role of altered activity of the autophagosome-lysosome pathway (ALP) in cardiac hypertrophy and heart failure. Although an early study suggested cardiac autophagy is increased and this increase is maladaptive to the heart subject to pressure overload, more recent reports overwhelmingly support that myocardial ALP insufficiency results from chronic pressure overload and contributes to maladaptive cardiac remodeling and heart failure...
June 2, 2017: American Journal of Physiology. Heart and Circulatory Physiology
https://www.readbyqxmd.com/read/28553639/role-of-endoplasmic-reticulum-stress-autophagy-and-inflammation-in-cardiovascular-disease
#13
REVIEW
Cheng Zhang, Taha Wasim Syed, Renjing Liu, Jun Yu
Cardiovascular diseases are a class of heart or blood vessels diseases, which are now considered to be the leading cause of death globally. A number of recent studies have reported key roles for inflammation in the progression of diseased vessels and systematic heart failure. In particular, endoplasmic reticulum (ER) stress, which is mechanistically implicated in inflammation and autophagy, has now been associated with pathophysiological states in the cardiovascular system. Autophagy has also been identified as an important process in the progression of multiple cardiovascular diseases such as in atherosclerosis plaque progression and ischemia and/or reperfusion...
2017: Frontiers in Cardiovascular Medicine
https://www.readbyqxmd.com/read/28551793/mitochondria-in-structural-and-functional-cardiac-remodeling
#14
Natalia Torrealba, Pablo Aranguiz, Camila Alonso, Beverly A Rothermel, Sergio Lavandero
The heart must function continuously as it is responsible for both supplying oxygen and nutrients throughout the entire body, as well as for the transport of waste products to excretory organs. When facing either a physiological or pathological increase in cardiac demand, the heart undergoes structural and functional remodeling as a means of adapting to increased workload. These adaptive responses can include changes in gene expression, protein composition, and structure of sub-cellular organelles involved in energy production and metabolism...
2017: Advances in Experimental Medicine and Biology
https://www.readbyqxmd.com/read/28526246/impaired-mitophagy-facilitates-mitochondrial-damage-in-danon-disease
#15
Sherin I Hashem, Anne N Murphy, Ajit S Divakaruni, Matthew L Klos, Bradley C Nelson, Emily C Gault, Teisha J Rowland, Cynthia N Perry, Yusu Gu, Nancy D Dalton, William H Bradford, Eric J Devaney, Kirk L Peterson, Kenneth L Jones, Matthew R G Taylor, Ju Chen, Neil C Chi, Eric D Adler
RATIONALE: Lysosomal associated membrane protein type-2 (LAMP-2) is a highly conserved, ubiquitous protein that is critical for autophagic flux. Loss of function mutations in the LAMP-2 gene cause Danon disease, a rare X-linked disorder characterized by developmental delay, skeletal muscle weakness, and severe cardiomyopathy. We previously found that human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) from Danon patients exhibited significant mitochondrial oxidative stress and apoptosis...
May 16, 2017: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/28515362/insulin-supplementation-attenuates-cancer-induced-cardiomyopathy-and-slows-tumor-disease-progression
#16
James T Thackeray, Stefan Pietzsch, Britta Stapel, Melanie Ricke-Hoch, Chun-Wei Lee, Jens P Bankstahl, Michaela Scherr, Jörg Heineke, Gesine Scharf, Arash Haghikia, Frank M Bengel, Denise Hilfiker-Kleiner
Advanced cancer induces fundamental changes in metabolism and promotes cardiac atrophy and heart failure. We discovered systemic insulin deficiency in cachectic cancer patients. Similarly, mice with advanced B16F10 melanoma (B16F10-TM) or colon 26 carcinoma (C26-TM) displayed decreased systemic insulin associated with marked cardiac atrophy, metabolic impairment, and function. B16F10 and C26 tumors decrease systemic insulin via high glucose consumption, lowering pancreatic insulin production and producing insulin-degrading enzyme...
May 18, 2017: JCI Insight
https://www.readbyqxmd.com/read/28494450/stachydrine-protects-against-pressure-overload-induced-cardiac-hypertrophy-by-suppressing-autophagy
#17
Tong-Tong Cao, Hui-Hua Chen, Zhiwei Dong, Yan-Wu Xu, Pei Zhao, Wei Guo, Hong-Chang Wei, Chen Zhang, Rong Lu
BACKGROUND: Autophagy is required for the maintenance of cardiomyocyte homeostasis. However, excessive autophagy plays a maladaptive role in pressure overload-induced heart failure. To identify mechanisms by which Stachydrine inhibits pressure overload-induced cardiac hypertrophy, we determined inhibitory activities against activation of NADPH oxidase, reactive oxygen species(ROS) production and excessive activation of autophagy. METHODS: Stachydrine was administered intragastrically to Wistar rats after Transverse aortic constriction(TAC) and H9c2 cells were treated with Stachydrine after Angiotension II stimulation...
2017: Cellular Physiology and Biochemistry
https://www.readbyqxmd.com/read/28493471/what-role-does-the-stress-response-have-in-congestive-heart-failure
#18
REVIEW
Ahmed Badreddin, Youssef Fady, Hamdy Attia, Mohamed Hafez, Ahmed Khairallah, Dina Johar, Larry Bernstein
This review is concerned with cardiac malfunction as a result of an imbalance in protein proteostasis, the homeostatic balance between protein removal and regeneration in a long remodeling process involving the endoplasmic reticulum (ER) and the unfolded protein response (UPR). The importance of this is of special significance with regard to cardiac function as a high energy requiring muscular organ that has a high oxygen requirement and is highly dependent on mitochondria. The importance of mitochondria is not only concerned with high energy dependence on mitochondrial electron transport, but it also has a role in the signaling between the mitochondria and the ER under stress...
May 11, 2017: Journal of Cellular Physiology
https://www.readbyqxmd.com/read/28487390/activation-of-the-amino-acid-response-pathway-blunts-the-effects-of-cardiac-stress
#19
Pu Qin, Pelin Arabacilar, Roberta E Bernard, Weike Bao, Alan R Olzinski, Yuanjun Guo, Hind Lal, Stephen H Eisennagel, Michael C Platchek, Wensheng Xie, Julius Del Rosario, Mohamad Nayal, Quinn Lu, Theresa Roethke, Christine G Schnackenberg, Fe Wright, Michael P Quaile, Wendy S Halsey, Ashley M Hughes, Ganesh M Sathe, George P Livi, Robert B Kirkpatrick, Xiaoyan A Qu, Deepak K Rajpal, Maria Faelth Savitski, Marcus Bantscheff, Gerard Joberty, Giovanna Bergamini, Thomas L Force, Gregory J Gatto, Erding Hu, Robert N Willette
BACKGROUND: The amino acid response (AAR) is an evolutionarily conserved protective mechanism activated by amino acid deficiency through a key kinase, general control nonderepressible 2. In addition to mobilizing amino acids, the AAR broadly affects gene and protein expression in a variety of pathways and elicits antifibrotic, autophagic, and anti-inflammatory activities. However, little is known regarding its role in cardiac stress. Our aim was to investigate the effects of halofuginone, a prolyl-tRNA synthetase inhibitor, on the AAR pathway in cardiac fibroblasts, cardiomyocytes, and in mouse models of cardiac stress and failure...
May 9, 2017: Journal of the American Heart Association
https://www.readbyqxmd.com/read/28455287/desmin-loss-and-mitochondrial-damage-precede-left-ventricular-systolic-failure-in-volume-overload-heart-failure
#20
Jason L Guichard, Michael Rogowski, Giulio Agnetti, Lianwu Fu, Pamela Powell, Chih-Chang Wei, James Collawn, Louis J Dell'Italia
Heart failure due to chronic volume overload (VO) in rats and humans is characterized by disorganization of the cardiomyocyte desmin/mitochondrial network. Here, we tested the hypothesis that desmin breakdown is an early and continuous process throughout VO. Male Sprague-Dawley rats had aortocaval fistula (ACF) or sham surgery and were examined 24 h and 4 and 12 wk later. Desmin/mitochondrial ultrastructure was examined by transmission electron microscopy (TEM) and immunohistochemistry (IHC). Protein and kinome analysis were performed in isolated cardiomyocytes, and desmin cleavage was assessed by mass spectrometry in left ventricular (LV) tissue...
July 1, 2017: American Journal of Physiology. Heart and Circulatory Physiology
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