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heart failure and autophagy

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https://www.readbyqxmd.com/read/28913665/role-of-noncoding-rnas-in-regulation-of-cardiac-cell-death-and-cardiovascular-diseases
#1
REVIEW
Yanhan Dong, Cuiyun Liu, Yanfang Zhao, Murugavel Ponnusamy, Peifeng Li, Kun Wang
Loss of functional cardiomyocytes is a major underlying mechanism for myocardial remodeling and heart diseases, due to the limited regenerative capacity of adult myocardium. Apoptosis, programmed necrosis, and autophagy contribute to loss of cardiac myocytes that control the balance of cardiac cell death and cell survival through multiple intricate signaling pathways. In recent years, non-coding RNAs (ncRNAs) have received much attention to uncover their roles in cell death of cardiovascular diseases, such as myocardial infarction, cardiac hypertrophy, and heart failure...
September 14, 2017: Cellular and Molecular Life Sciences: CMLS
https://www.readbyqxmd.com/read/28874825/knockout-of-the-atpase-inhibitory-factor-1-protects-the-heart-from-pressure-overload-induced-cardiac-hypertrophy
#2
Kevin Yang, Qinqiang Long, Kamalamma Saja, Fengyuan Huang, Steven M Pogwizd, Lufang Zhou, Masasuke Yoshida, Qinglin Yang
Mitochondrial ATP synthase catalyzes the coupling of oxidative phosphorylation. Under pathological conditions, ATP synthase hydrolyzes ATP to replenish protons from the matrix into the intermembrane space, sustaining mitochondrial membrane potential. ATPase inhibitory factor 1 (IF1) is a nuclear-encoded, ATP synthase-interacting protein that selectively inhibits the hydrolysis activity of ATP synthase, which may render the protective role of IF1 in ischemic hearts. However, the in vivo cardiac function of IF1 and the potential therapeutic application targeting IF1 remain obscure...
September 5, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28871076/knockdown-of-microrna-122-protects-h9c2-cardiomyocytes-from-hypoxia-induced-apoptosis-and-promotes-autophagy
#3
Zaiwei Zhang, Hu Li, Shasha Chen, Ying Li, Zhiyuan Cui, Jie Ma
BACKGROUND Acute myocardial infarction (AMI) is a severe disease causing heart failure and sudden death. Studies indicate that microRNAs (miRNAs) are involved in the pathophysiology of AMI. In the present study, we carefully explored the effects of miR-122 on myocardial hypoxia injury and its possible underlying mechanism. MATERIAL AND METHODS miR-122 expression was analyzed in H9c2 cardiomyocytes after being transfected with miR-122 mimic, ASO-miR-122, or negative control. Cell viability and apoptosis were investigated by CCK-8 assays and flow cytometry analysis, respectively...
September 5, 2017: Medical Science Monitor: International Medical Journal of Experimental and Clinical Research
https://www.readbyqxmd.com/read/28842527/mechanisms-contributing-to-cardiac-remodelling
#4
REVIEW
Qing-Qing Wu, Yang Xiao, Yuan Yuan, Zhen-Guo Ma, Hai-Han Liao, Chen Liu, Jin-Xiu Zhu, Zheng Yang, Wei Deng, Qi-Zhu Tang
Cardiac remodelling is classified as physiological (in response to growth, exercise and pregnancy) or pathological (in response to inflammation, ischaemia, ischaemia/reperfusion (I/R) injury, biomechanical stress, excess neurohormonal activation and excess afterload). Physiological remodelling of the heart is characterized by a fine-tuned and orchestrated process of beneficial adaptations. Pathological cardiac remodelling is the process of structural and functional changes in the left ventricle (LV) in response to internal or external cardiovascular damage or influence by pathogenic risk factors, and is a precursor of clinical heart failure (HF)...
September 15, 2017: Clinical Science (1979-)
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
#5
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 embolism until hemodynamic compromise followed by dobutamine infusion for hemodynamic restoration before 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
#6
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
#7
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, antitumor agents that are capable of killing cells were investigated. Testing of various antitumor 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...
October 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
#8
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
#9
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
#10
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
#11
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
#12
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
#13
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
#14
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 characterize 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 wk after myocardial infarction...
August 3, 2017: Autophagy
https://www.readbyqxmd.com/read/28590260/ghrelin-and-autophagy
#15
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
#16
REVIEW
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 that cardiac autophagy is increased and that this increase is maladaptive to the heart subject to pressure overload, more recent reports have overwhelmingly supported that myocardial ALP insufficiency results from chronic pressure overload and contributes to maladaptive cardiac remodeling and heart failure...
August 1, 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
#17
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
#18
REVIEW
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
#19
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
#20
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
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