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heart failure and endoplasmic reticulum

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...
December 2, 2016: Cell Death and Differentiation
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
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
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
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
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
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
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...
July 21, 2016: Environmental Toxicology
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
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
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
Y Liu, S Y Qi, L S Ru, C Ding, H J Wang, A Y Li, B Y Xu, G H Zhang, D M Wang
OBJECTIVE: Endoplasmic reticulum (ER) stress plays an important role in ischemia-mediated cell death. The aim of the current study is to investigate the effects of salubrinal (Sal), a selective eIF2a dephosphorylation inhibitor, on heart failure rats and related mechanisms. METHODS: Heart failure was induced by coronary artery ligation (MI) in adult male Sprague-Dawley rats. To ensure comparable MI sizes post coronary artery ligation on various groups, echocardiography examination was performed before and 30 minutes after ligation in MI groups...
June 24, 2016: Zhonghua Xin Xue Guan Bing za Zhi
Luiz H M Bozi, Paulo R Jannig, Natale Rolim, Vanessa A Voltarelli, Paulo M M Dourado, Ulrik Wisløff, Patricia C Brum
Cardiac endoplasmic reticulum (ER) stress through accumulation of misfolded proteins plays a pivotal role in cardiovascular diseases. In an attempt to reestablish ER homoeostasis, the unfolded protein response (UPR) is activated. However, if ER stress persists, sustained UPR activation leads to apoptosis. There is no available therapy for ER stress relief. Considering that aerobic exercise training (AET) attenuates oxidative stress, mitochondrial dysfunction and calcium imbalance, it may be a potential strategy to reestablish cardiac ER homoeostasis...
June 16, 2016: Journal of Cellular and Molecular Medicine
Quanlu Duan, Li Ni, Peihua Wang, Chen Chen, Lei Yang, Ben Ma, Wei Gong, Zhejun Cai, Ming-Hui Zou, Dao Wen Wang
Endoplasmic reticulum (ER) stress has been reported to be involved in many cardiovascular diseases such as atherosclerosis, diabetes, myocardial ischemia, and hypertension that ultimately result in heart failure. XBP1 is a key ER stress signal transducer and an important pro-survival factor of the unfolded protein response (UPR) in mammalian cells. The aim of this study was to establish a role for XBP1 in the deregulation of pro-angiogenic factor VEGF expression and potential regulatory mechanisms in hypertrophic and failing heart...
August 2016: Aging Cell
Xiaomin Zhou, Qing Xin, Yilin Wang, Yajun Zhao, Hua Chai, Xia Huang, Xiexin Tao, Ming Zhao
BACKGROUND: Viral myocarditis is initiated by viral infection of myocardial tissue leading to dilated cardiomyopathy and congestive heart failure. Recent studies have linked viral myocarditis with dysfunctions in endoplasmic reticulum (ER) mediated Ca(2+) homeostasis and the unfolded protein response (UPR). Currently there are no effective treatments for this viral infection. METHODS: We employed the use of a well-characterized pathogen coxsackievirus B3 (CVB3) to induce mouse viral myocarditis...
January 2016: Acta Cardiologica Sinica
Remya Sreedhar, Vijayasree V Giridharan, Somasundaram Arumugam, Vengadeshprabhu Karuppagounder, Suresh S Palaniyandi, Prasanna Krishnamurthy, Joao Quevedo, Kenichi Watanabe, Tetsuya Konishi, Rajarajan A Thandavarayan
Heart failure is typically related to aging as there is a definite relationship between age-related changes in the heart and the pathogenesis of heart failure. We have previously reported the involvement of p38 mitogen-activated protein kinase protein in cardiac function using animal models of heart failure. To further understand its relationship with aging-induced heart failure, we have compared its expression in the hearts of senescence accelerated-prone (SAMP8) mice and their control (SAMR1) with normal aging behavior...
July 8, 2016: BioFactors
Adriana Izquierdo-Lahuerta, Cristina Martínez-García, Gema Medina-Gómez
In the last few decades, rapid changes in lifestyle have led to an alarming increase in the prevalence of obesity and obesity-associated complications. Obese patients are at increased risk of developing hypertension, heart disease, insulin resistance, dyslipidemia, type 2 diabetes and kidney disease. The surplus of calories is normally stored as triglycerides in adipose tissue. However, excess lipids can also accumulate ectopically in other organs, including the kidney, contributing to their damage through toxic processes named lipotoxicity...
October 2016: Journal of Nephrology
Luigi X Cubeddu
Risk of severe and fatal ventricular arrhythmias, presenting as Torsade de Pointes (TdP), is increased in congenital and acquired forms of long QT syndromes (LQTS). Drug-induced inhibition of K+ currents, IKs, IKr, IK1, and/or Ito, delay repolarization, prolong QT, and increase the risk of TdP. Drug-induced interference with IKr is the most common cause of acquired LQTS/TdP. Multiple drugs bind to KNCH2-hERG-K+ channels affecting IKr, including antiarrythmics, antibiotics, antivirals, azole-antifungals, antimalarials, anticancer, antiemetics, prokinetics, antipsychotics, and antidepressants...
2016: Current Cardiology Reviews
Hai Ying Fu, Shoji Sanada, Takashi Matsuzaki, Yulin Liao, Keiji Okuda, Masaki Yamato, Shota Tsuchida, Ryo Araki, Yoshihiro Asano, Hiroshi Asanuma, Masanori Asakura, Brent A French, Yasushi Sakata, Masafumi Kitakaze, Tetsuo Minamino
RATIONALE: Doxorubicin is an effective chemotherapeutic agent for cancer, but its use is often limited by cardiotoxicity. Doxorubicin causes endoplasmic reticulum (ER) dilation in cardiomyocytes, and we have demonstrated that ER stress plays important roles in the pathophysiology of heart failure. OBJECTIVE: We evaluated the role of ER stress in doxorubicin-induced cardiotoxicity and examined whether the chemical ER chaperone could prevent doxorubicin-induced cardiac dysfunction...
March 4, 2016: Circulation Research
Barry Greenberg, Javed Butler, G Michael Felker, Piotr Ponikowski, Adriaan A Voors, Akshay S Desai, Denise Barnard, Alain Bouchard, Brian Jaski, Alexander R Lyon, Janice M Pogoda, Jeffrey J Rudy, Krisztina M Zsebo
BACKGROUND: Sarcoplasmic/endoplasmic reticulum Ca(2+)-ATPase (SERCA2a) activity is deficient in the failing heart. Correction of this abnormality by gene transfer might improve cardiac function. We aimed to investigate the clinical benefits and safety of gene therapy through infusion of adeno-associated virus 1 (AAV1)/SERCA2a in patients with heart failure and reduced ejection fraction. METHODS: We did this randomised, multinational, double-blind, placebo-controlled, phase 2b trial at 67 clinical centres and hospitals in the USA, Europe, and Israel...
March 19, 2016: Lancet
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