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heart failure and endoplasmic reticulum

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https://www.readbyqxmd.com/read/28296550/protective-effects-of-salusin-%C3%AE-and-salusin-%C3%AE-on-renal-ischemia-reperfusion-damage-and-their-levels-in-ischemic-acute-renal-failure
#1
M Cakir, H Duzova, A Taslidere, G Orhan, F Ozyalin
Salusin-α and salusin-β are expressed in many tissues including the central nervous system, vessels and kidneys; they have been shown to decrease endoplasmic reticulum stress during heart ischemia/reperfusion (I/R) and to decrease apoptosis. We investigated the relation of salusin-α and salusin-β levels to acute ischemic renal failure. We also investigated whether these peptides are protective against renal I/R damage. Fifty-three rats were divided into six groups: control, I/R, I/R + salusin-α1, I/R + salusin-α10, I/R + salusin-β1 and I/R + salusin-β10...
2017: Biotechnic & Histochemistry: Official Publication of the Biological Stain Commission
https://www.readbyqxmd.com/read/28275246/sarcoplasmic-reticulum-mitochondria-communication-in-cardiovascular-pathophysiology
#2
REVIEW
Camila Lopez-Crisosto, Christian Pennanen, Cesar Vasquez-Trincado, Pablo E Morales, Roberto Bravo-Sagua, Andrew F G Quest, Mario Chiong, Sergio Lavandero
Repetitive, calcium-mediated contractile activity renders cardiomyocytes critically dependent on a sustained energy supply and adequate calcium buffering, both of which are provided by mitochondria. Moreover, in vascular smooth muscle cells, mitochondrial metabolism modulates cell growth and proliferation, whereas cytosolic calcium levels regulate the arterial vascular tone. Physical and functional communication between mitochondria and sarco/endoplasmic reticulum and balanced mitochondrial dynamics seem to have a critical role for optimal calcium transfer to mitochondria, which is crucial in calcium homeostasis and mitochondrial metabolism in both types of muscle cells...
March 9, 2017: Nature Reviews. Cardiology
https://www.readbyqxmd.com/read/28223472/overexpression-of-sarcoendoplasmic-reticulum-calcium-atpase-2a-promotes-cardiac-sympathetic-neurotransmission-via-abnormal-endoplasmic-reticulum-and-mitochondria-ca-2-regulation
#3
Julia Shanks, Neil Herring, Errin Johnson, Kun Liu, Dan Li, David J Paterson
Reduced cardiomyocyte excitation-contraction coupling and downregulation of the SERCA2a (sarcoendoplasmic reticulum calcium ATPase 2a) is associated with heart failure. This has led to viral transgene upregulation of SERCA2a in cardiomyocytes as a treatment. We hypothesized that SERCA2a gene therapy expressed under a similar promiscuous cytomegalovirus promoter could also affect the cardiac sympathetic neural axis and promote sympathoexcitation. Stellate neurons were isolated from 90 to 120 g male, Sprague-Dawley, Wistar Kyoto, and spontaneously hypertensive rats...
April 2017: Hypertension
https://www.readbyqxmd.com/read/28218221/gene-expressions-underlying-mishandled-calcium-clearance-and-elevated-generation-of-reactive-oxygen-species-in-the-coronary-artery-smooth-muscle-cells-of-chronic-heart-failure-rats
#4
Liang Ding, Xian-Xiu Su, Wen-Hui Zhang, Yu-Xiang Xu, Xue-Feng Pan
BACKGROUND: The calcium clearance and reactive oxygen species (ROS) generations in the coronary artery smooth muscle cells in chronic heart failure (HF) have not been fully investigated. Therefore, we attempted to understand the gene expressions underlying the mishandling of calcium clearance and the accumulations of ROS. METHODS: We initially established an animal model of chronic HF by making the left anterior descending coronary artery ligation (CAL) in rats, and then isolated the coronary artery vascular smooth muscle cells from the ischemic and the nonischemic parts of the coronary artery vessels in 12 weeks after CAL operation...
2017: Chinese Medical Journal
https://www.readbyqxmd.com/read/28208629/effects-of-the-activin-a-follistatin-system-on-myocardial-cell-apoptosis-through-the-endoplasmic-reticulum-stress-pathway-in-heart-failure
#5
Miao Liu, Cuiying Mao, Jiayu Li, Fanglei Han, Ping Yang
BACKGROUND: A previous study suggested that activin A inhibited myocardial cell apoptosis. This study thus aimed to explore the effects of the activin A-follistatin system on myocardial cell apoptosis in heart failure (HF) rats in order to determine whether or not the mechanism operates through the endoplasmic reticulum stress (ERS) pathway. METHODS: Myocardial infarction (MI) by vascular deprivation was used to induce HF. The enzyme-linked immunosorbent assay was used to detect activin A, follistatin and brain natriuretic peptide (BNP) contents in serum...
February 10, 2017: International Journal of Molecular Sciences
https://www.readbyqxmd.com/read/28176614/acanthomatous-ameloblastoma-with-atypical-foci-in-five-dogs
#6
Jennifer L Malmberg, Elizabeth W Howerth, Barb E Powers, Paula A Schaffer
Acanthomatous ameloblastoma is a common, locally invasive, nonmetastasizing tumor of the canine oral cavity. The long-term prognosis for canine acanthomatous ameloblastoma is good if complete excision can be achieved, usually by maxillectomy or mandibulectomy. A variant of acanthomatous ameloblastoma with atypical foci was noted in 5 dogs. There was no age, breed, or sex predisposition. Atypical cells were pleomorphic with a high mitotic rate. They were immunohistochemically negative for cytokeratin, vimentin, melan A, PNL2, CD3, Pax5, CD18, chromogranin A, and synaptophysin...
January 1, 2017: Journal of Veterinary Diagnostic Investigation
https://www.readbyqxmd.com/read/28151473/knockout-of-eva1a-leads-to-rapid-development-of-heart-failure-by-impairing-autophagy
#7
Shu Zhang, Xin Lin, Ge Li, Xue Shen, Di Niu, Guang Lu, Xin Fu, Yingyu Chen, Ming Cui, Yun Bai
EVA1A (Eva-1 homologue A) is a novel lysosome and endoplasmic reticulum-associated protein that can regulate cell autophagy and apoptosis. Eva1a is expressed in the myocardium, but its function in myocytes has not yet been investigated. Therefore, we generated inducible, cardiomyocyte-specific Eva1a knockout mice with an aim to determine the role of Eva1a in cardiac remodelling in the adult heart. Data from experiments showed that loss of Eva1a in the adult heart increased cardiac fibrosis, promoted cardiac hypertrophy, and led to cardiomyopathy and death...
February 2, 2017: Cell Death & Disease
https://www.readbyqxmd.com/read/28134413/the-function-and-significance-of-sera2a-in-congestive-heart-failure-an-analysis-of-gene-therapy-trials
#8
REVIEW
Pei Wu, Yuting Zhai, Dongye Li
Congestive heart failure (CHF) is a widespread disease that has a negative impact on health, worldwide. Despite advances in therapies, morbidity, mortality and hospital discharges due to CHF remain high. Advances in the understanding of the pathophysiological mechanisms of CHF and the development of gene transfer technology have made gene therapy a realistic potential therapeutic method for CHF. Among the various potential targets, sarco-endoplasmic reticulum Ca2+-ATPase 2a (SERCA2a), which is an important protein in the regulation of Ca2+ cycling, has piqued the interest of many researchers...
January 30, 2017: Histology and Histopathology
https://www.readbyqxmd.com/read/28120277/protein-quality-control-dysfunction-in-cardiovascular-complications-induced-by-anti-cancer-drugs
#9
REVIEW
Hai Ying Fu, Mikio Mukai, Nobuhisa Awata, Yasushi Sakata, Masatsugu Hori, Tetsuo Minamino
Cardiovascular complications, including heart failure, hypertension, ischemic syndromes and venous thromboembolism, have been identified in patients treated with anti-cancer drugs. Oxidative stress, mitochondrial dysfunction and DNA synthesis inhibition are considered to be responsible for the cardiotoxicity induced by these agents. Protein quality control (PQC) has 3 major components, including the endoplasmic reticulum (ER), the ubiquitin-proteasome system (UPS) and the autophagy-lysosome system, and participates in protein folding and degradation to maintain protein homeostasis...
February 2017: Cardiovascular Drugs and Therapy
https://www.readbyqxmd.com/read/27911441/sirt1-protects-the-heart-from-er-stress-induced-cell-death-through-eif2%C3%AE-deacetylation
#10
Alexandre Prola, Julie Pires Da Silva, Arnaud Guilbert, Lola Lecru, Jérôme Piquereau, Maxance Ribeiro, Philippe Mateo, Mélanie Gressette, Dominique Fortin, Céline Boursier, Cindy Gallerne, Anaïs Caillard, Jane-Lise Samuel, Hélène François, David A Sinclair, Pierre Eid, Renée Ventura-Clapier, Anne Garnier, Christophe Lemaire
Over the past decade, endoplasmic reticulum (ER) stress has emerged as an important mechanism involved in the pathogenesis of cardiovascular diseases including heart failure. Cardiac therapy based on ER stress modulation is viewed as a promising avenue toward effective therapies for the diseased heart. Here, we tested whether sirtuin-1 (SIRT1), a NAD(+)-dependent deacetylase, participates in modulating ER stress response in the heart. Using cardiomyocytes and adult-inducible SIRT1 knockout mice, we demonstrate that SIRT1 inhibition or deficiency increases ER stress-induced cardiac injury, whereas activation of SIRT1 by the SIRT1-activating compound STAC-3 is protective...
February 2017: Cell Death and Differentiation
https://www.readbyqxmd.com/read/27815070/direct-detection-of-serca-calcium-transport-and-small-molecule-inhibition-in-giant-unilamellar-vesicles
#11
Tengfei Bian, Joseph M Autry, Denise Casemore, Ji Li, David D Thomas, Gaohong He, Chengguo Xing
We have developed a charge-mediated fusion method to reconstitute the sarco/endoplasmic reticulum Ca(2+)-ATPase (SERCA) in giant unilamellar vesicles (GUV). Intracellular Ca(2+) transport by SERCA controls key processes in human cells such as proliferation, signaling, and contraction. Small-molecule effectors of SERCA are urgently needed as therapeutics for Ca(2+) dysregulation in human diseases including cancer, diabetes, and heart failure. Here we report the development of a method for efficiently reconstituting SERCA in GUV, and we describe a streamlined protocol based on optimized parameters (e...
December 9, 2016: Biochemical and Biophysical Research Communications
https://www.readbyqxmd.com/read/27763637/nogo-c-regulates-cardiomyocyte-apoptosis-during-mouse-myocardial-infarction
#12
Shi Jia, Xue Qiao, Jingjing Ye, Xuan Fang, Chunling Xu, Yangpo Cao, Ming Zheng
Myocardial infarction is caused by insufficient coronary blood supply, which leads to myocardial damage and eventually the heart failure. Molecular mechanisms associated with the loss of cardiomyocytes during myocardial infarction (MI) and ischemia-related cardiac diseases are not yet fully understood. Nogo-C is an endoplasmic reticulum protein ubiquitously expressed in tissues including in the heart, however, the cardiac function of Nogo-C is still unknown. In the present study, we found that Nogo-C was upregulated in mouse hearts after MI, and hypoxic treatments also increased Nogo-C protein level in cardiomyocytes...
October 20, 2016: Cell Death & Disease
https://www.readbyqxmd.com/read/27667442/histone-deacetylase-inhibitor-phenylbutyrate-exaggerates-heart-failure-in-pressure-overloaded-mice-independently-of-hdac-inhibition
#13
Jing Ma, Tao Luo, Zhi Zeng, Haiying Fu, Yoshihiro Asano, Yulin Liao, Tetsuo Minamino, Masafumi Kitakaze
4-Sodium phenylbutyrate (PBA) has been reported to inhibit endoplasmic reticulum stress and histone deacetylation (HDAC), both of which are novel therapeutic targets for cardiac hypertrophy and heart failure. However, it is unclear whether PBA can improve heart function. Here, we tested the effects of PBA and some other HDAC inhibitors on cardiac dysfunction induced by pressure overload. Transverse aortic constriction (TAC) was performed on male C57BL/6 mice. PBA treatment (100 mg/kg, 6 weeks) unexpectedly led to a higher mortality, exacerbated cardiac remodelling and dysfunction...
September 26, 2016: Scientific Reports
https://www.readbyqxmd.com/read/27536244/reactive-oxygen-species-endoplasmic-reticulum-stress-and-mitochondrial-dysfunction-the-link-with-cardiac-arrhythmogenesis
#14
REVIEW
Gary Tse, Bryan P Yan, Yin W F Chan, Xiao Yu Tian, Yu Huang
BACKGROUND: Cardiac arrhythmias represent a significant problem globally, leading to cerebrovascular accidents, myocardial infarction, and sudden cardiac death. There is increasing evidence to suggest that increased oxidative stress from reactive oxygen species (ROS), which is elevated in conditions such as diabetes and hypertension, can lead to arrhythmogenesis. METHOD: A literature review was undertaken to screen for articles that investigated the effects of ROS on cardiac ion channel function, remodeling and arrhythmogenesis...
2016: Frontiers in Physiology
https://www.readbyqxmd.com/read/27496879/endoplasmic-reticulum-stress-increases-brain-mapk-signaling-inflammation-and-renin-angiotensin-system-activity-and-sympathetic-nerve-activity-in-heart-failure
#15
Shun-Guang Wei, Yang Yu, Robert M Weiss, Robert B Felder
We previously reported that endoplasmic reticulum (ER) stress is induced in the subfornical organ (SFO) and the hypothalamic paraventricular nucleus (PVN) of heart failure (HF) rats and is reduced by inhibition of mitogen-activated protein kinase (MAPK) signaling. The present study further examined the relationship between brain MAPK signaling, ER stress, and sympathetic excitation in HF. Sham-operated (Sham) and HF rats received a 4-wk intracerebroventricular (ICV) infusion of vehicle (Veh) or the ER stress inhibitor tauroursodeoxycholic acid (TUDCA, 10 μg/day)...
October 1, 2016: American Journal of Physiology. Heart and Circulatory Physiology
https://www.readbyqxmd.com/read/27470514/essential-role-of-smooth-muscle-stim1-in-hypertension-and-cardiovascular-dysfunction
#16
Modar Kassan, Karima Ait-Aissa, Eman Radwan, Vishal Mali, Samuel Haddox, Mohanad Gabani, Wei Zhang, Souad Belmadani, Kaikobad Irani, Mohamed Trebak, Khalid Matrougui
OBJECTIVES: Chronic hypertension is the most critical risk factor for cardiovascular disease, heart failure, and stroke. APPROACH AND RESULTS: Here we show that wild-type mice infused with angiotensin II develop hypertension, cardiac hypertrophy, perivascular fibrosis, and endothelial dysfunction with enhanced stromal interaction molecule 1 (STIM1) expression in heart and vessels. All these pathologies were significantly blunted in mice lacking STIM1 specifically in smooth muscle (Stim1(SMC-/-))...
September 2016: Arteriosclerosis, Thrombosis, and Vascular Biology
https://www.readbyqxmd.com/read/27442881/toll-like-receptor-4-ablation-rescues-against-paraquat-triggered-myocardial-dysfunction-role-of-er-stress-and-apoptosis
#17
Yonghong Lei, Xue Li, Fang Yuan, Lu Liu, Juan Zhang, Yanping Yang, Jieqiong Zhao, Yan Han, Jun Ren, Xiaobing Fu
Paraquat is a nitrogen herbicide imposing severe organ toxicity in human leading to acute lung injury and heart failure. The present study was designed to examine the impact of ablation of the innate proinflammatory mediator toll-like receptor 4 (TLR4) in paraquat-induced cardiac contractile dysfunction and the underlying mechanisms involved with a focus on endoplasmic reticulum (ER) stress and apoptosis. Adult male wild-type (WT) and TLR4 knockout (TLR4(-/-) ) mice were challenged with paraquat (45 mg/kg, i...
February 2017: Environmental Toxicology
https://www.readbyqxmd.com/read/27441395/inhibition-of-the-unfolded-protein-response-mechanism-prevents-cardiac-fibrosis
#18
Jody Groenendyk, Dukgyu Lee, Joanna Jung, Jason R B Dyck, Gary D Lopaschuk, Luis B Agellon, Marek Michalak
BACKGROUND: Cardiac fibrosis attributed to excessive deposition of extracellular matrix proteins is a major cause of heart failure and death. Cardiac fibrosis is extremely difficult and challenging to treat in a clinical setting due to lack of understanding of molecular mechanisms leading to cardiac fibrosis and effective anti-fibrotic therapies. The objective in this study was to examine whether unfolded protein response (UPR) pathway mediates cardiac fibrosis and whether a pharmacological intervention to modulate UPR can prevent cardiac fibrosis and preserve heart function...
2016: PloS One
https://www.readbyqxmd.com/read/27402067/effect-of-heart-failure-on-catecholamine-granule-morphology-and-storage-in-chromaffin-cells
#19
Sushil K Mahata, Hong Zheng, Sumana Mahata, Xuefei Liu, Kaushik P Patel
One of the key mechanisms involved in sympathoexcitation in chronic heart failure (HF) is the activation of the adrenal glands. Impact of the elevated catecholamines on the hemodynamic parameters has been previously demonstrated. However, studies linking the structural effects of such overactivation with secretory performance and cell metabolism in the adrenomedullary chromaffin cells in vivo have not been previously reported. In this study, HF was induced in male Sprague-Dawley rats by ligation of the left coronary artery...
September 2016: Journal of Endocrinology
https://www.readbyqxmd.com/read/27393458/blockade-of-receptor-for-advanced-glycation-end-products-protects-against-systolic-overload-induced-heart-failure-after-transverse-aortic-constriction-in-mice
#20
Yu Liu, Manli Yu, Zhigang Zhang, Yunhua Yu, Qi Chen, Wei Zhang, Xianxian Zhao
Heart failure is the consequence of sustained, abnormal neurohormonal and mechanical stress and remains a leading cause of death worldwide. The aim of this work was to identify whether blockade of receptor for advanced glycation end products (RAGE) protected against systolic overload-induced heart failure and investigate the possible underlying mechanism. It was found that RAGE mRNA and protein expression was up-regulated in cardiac tissues from mice subjected to pressure overload by transverse aortic constriction (TAC)...
November 15, 2016: European Journal of Pharmacology
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