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heart and endoplasmic reticulum

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https://www.readbyqxmd.com/read/28934226/pathological-alterations-in-liver-injury-following-congestive-heart-failure-induced-by-volume-overload-in-rats
#1
Mohammed Shaqura, Doaa M Mohamed, Noureddin B Aboryag, Lama Bedewi, Lukas Dehe, Sascha Treskatsch, Mehdi Shakibaei, Michael Schäfer, Shaaban A Mousa
Heart failure has emerged as a disease with significant public health implications. Following progression of heart failure, heart and liver dysfunction are frequently combined in hospitalized patients leading to increased morbidity and mortality. Here, we investigated the underlying pathological alterations in liver injury following heart failure. Heart failure was induced using a modified infrarenal aortocaval fistula (ACF) in male Wistar rats. Sham operated and ACF rats were compared for their morphometric and hemodynamic data, for histopathological and ultrastructural changes in the liver as well as differences in the expression of apoptotic factors...
2017: PloS One
https://www.readbyqxmd.com/read/28931551/endoplasmic-reticulum-membrane-protein-complex-subunit-10-emc10-is-a-bone-marrow-derived-angiogenic-growth-factor-promoting-tissue-repair-after-myocardial-infarction
#2
Marc R Reboll, Mortimer Korf-Klingebiel, Stefanie Klede, Felix Polten, Eva Brinkmann, Ines Reimann, Hans-Joachim Schönfeld, Maria Bobadilla, Jan Faix, George Kensah, Ina Gruh, Michael Klintschar, Matthias Gaestel, Hans W Niessen, Andreas Pich, Johann Bauersachs, Joseph A Gogos, Yong Wang, Kai C Wollert
Background -Clinical trials of bone marrow cell (BMC)-based therapies after acute myocardial infarction (MI) have produced mostly neutral results. Treatment with specific BMC-derived secreted proteins may provide an alternative biologic approach to improving tissue repair and heart function after MI. We recently performed a bioinformatic secretome analysis in BMCs from patients with acute MI and discovered a poorly characterized secreted protein, endoplasmic reticulum membrane protein complex subunit 10 (EMC10), showing activity in an angiogenic screen...
September 20, 2017: Circulation
https://www.readbyqxmd.com/read/28903365/protective-effects-of-circulating-microvesicles-derived-from-myocardial-ischemic-rats-on-apoptosis-of-cardiomyocytes-in-myocardial-ischemia-reperfusion-injury
#3
Yao Wang, Su Wei, Yi-Lu Wang, Miao Liu, Man Shang, Qi Zhang, Yan-Na Wu, Ming-Lin Liu, Jun-Qiu Song, Yan-Xia Liu
OBJECTIVE: To investigate the effects of circulating microvesicles derived from myocardial ischemia (I-MVs) on apoptosis in myocardial ischemia/reperfusion (I/R) injury in rats. METHODS: I-MVs from rats undergoing myocardial left anterior descending (LAD) coronary artery ligation were isolated by ultracentrifugation from circulating blood and characterized by flow cytometry. I-MVs were administered intravenously (4.8 mg/kg) at 5 min before reperfusion procedure in I/R injury model which was induced by 30-min of ischemia and 120-min of reperfusion of LAD in rats...
August 15, 2017: Oncotarget
https://www.readbyqxmd.com/read/28901522/glutathione-system-in-wolfram-syndrome-1%C3%A2-deficient-mice
#4
Rando Porosk, Kalle Kilk, Riina Mahlapuu, Anton Terasmaa, Ursel Soomets
Wolfram syndrome 1 (WS) is a rare neurodegenerative disease that is caused by mutations in the Wolfram syndrome 1 (WFS1) gene, which encodes the endoplasmic reticulum (ER) glycoprotein wolframin. The pathophysiology of WS is ER stress, which is generally considered to induce oxidative stress. As WS has a well‑defined monogenetic origin and a model for chronic ER stress, the present study aimed to characterize how glutathione (GSH), a major intracellular antioxidant, was related to the disease and its progression...
August 31, 2017: Molecular Medicine Reports
https://www.readbyqxmd.com/read/28875043/the-role-of-endoplasmic-reticulum-stress-in-cardiovascular-disease-and-exercise
#5
REVIEW
Junyoung Hong, Kwangchan Kim, Jong-Hee Kim, Yoonjung Park
Endoplasmic reticulum (ER) stress, which is highly associated with cardiovascular disease, is triggered by a disturbance in ER function because of protein misfolding or an increase in protein secretion. Prolonged disruption of ER causes ER stress and activation of the unfolded protein response (UPR) and leads to various diseases. Eukaryotic cells respond to ER stress via three major sensors that are bound to the ER membrane: activating transcription factor 6 (ATF6), inositol-requiring protein 1α (IRE1α), and protein kinase RNA-like ER kinase (PERK)...
2017: International Journal of Vascular Medicine
https://www.readbyqxmd.com/read/28860710/alginate-oligosaccharide-alleviates-myocardial-reperfusion-injury-by-inhibiting-nitrative-and-oxidative-stress-and-endoplasmic-reticulum-stress-mediated-apoptosis
#6
Jun-Jie Guo, Feng-Qiang Xu, Yong-Hong Li, Jian Li, Xin Liu, Xiao-Fan Wang, Long-Gang Hu, Yi An
Alginate oligosaccharide (AOS) has recently demonstrated the ability to protect against acute doxorubicin cardiotoxicity and neurodegenerative disorders by inhibiting oxidative stress and endoplasmic reticulum (ER) stress-mediated apoptosis, which are both involved in myocardial ischemia/reperfusion (I/R) injury. In the present study, we investigated whether pretreatment with AOS protects against myocardial I/R injury in mice and explored potential cardioprotective mechanisms. AOS pretreatment significantly decreased the infarct size, reduced the cardiac troponin-I concentration, and ameliorated the cardiac dysfunction...
2017: Drug Design, Development and Therapy
https://www.readbyqxmd.com/read/28858301/activation-of-aldehyde-dehydrogenase-2-slows-down-the-progression-of-atherosclerosis-via-attenuation-of-er-stress-and-apoptosis-in-smooth-muscle-cells
#7
Mei-Yan Yang, Ya-Bin Wang, Bo Han, Bo Yang, Yu-Wei Qiang, Yan Zhang, Zhao Wang, Xu Huang, Jie Liu, Yun-Dai Chen, Jun Ren, Feng Cao, Yong Xu
Aldehyde dehydrogenase 2 (ALDH2) is a key mitochondrial enzyme in the metabolism of aldehydes and may have beneficial cardiovascular effects for conditions such as cardiac hypertrophy, heart failure, myocardial I/R injury, reperfusion, arrhythmia, coronary heart disease and atherosclerosis. In this study we investigated the role of ALDH2 in the progression of atherosclerosis and the underlying mechanisms, with a focus on endoplasmic reticulum (ER) stress. A clinical study was performed in 248 patients with coronary heart disease...
August 31, 2017: Acta Pharmacologica Sinica
https://www.readbyqxmd.com/read/28846567/chronic-kidney-disease-exacerbates-myocardial-ischemia-reperfusion-injury-role-of-endoplasmic-reticulum-stress-mediated-apoptosis
#8
Junjie Guo, Jianbing Zhu, Leilei Ma, Hongtao Shi, Jiachang Hu, Shuning Zhang, Lei Hou, Fengqiang Xu, Yi An, Haichu Yu, Junbo Ge
Chronic kidney disease (CKD) is known to exacerbate myocardial ischemia reperfusion (IR) injury. However, the underlying mechanisms are still not well understood. Despite various strategies for cardioprotection, limited studies have been focused on the prevention of CKD-induced myocardial susceptibility to IR injury. Here, we hypothesized that excessive endoplasmic reticulum (ER) stress-mediated apoptosis involved in myocardial IR injury in CKD mice and pretreatment with chemical ER chaperone rendered the heart resistant to myocardial IR injury in the setting of CKD...
August 25, 2017: Shock
https://www.readbyqxmd.com/read/28842527/mechanisms-contributing-to-cardiac-remodelling
#9
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/28801668/exercise-leads-to-unfavourable-cardiac-remodelling-and-enhanced-metabolic-homeostasis-in-obese-mice-with-cardiac-and-skeletal-muscle-autophagy-deficiency
#10
Zhen Yan, Ana Kronemberger, Jay Blomme, Jarrod A Call, Hannah M Caster, Renata O Pereira, Henan Zhao, Vitor U de Melo, Rhianna C Laker, Mei Zhang, Vitor A Lira
Autophagy is stimulated by exercise in several tissues; yet the role of skeletal and cardiac muscle-specific autophagy on the benefits of exercise training remains incompletely understood. Here, we determined the metabolic impact of exercise training in obese mice with cardiac and skeletal muscle disruption of the Autophagy related 7 gene (Atg7(h&mKO)). Muscle autophagy deficiency did not affect glucose clearance and exercise capacity in lean adult mice. High-fat diet in sedentary mice led to endoplasmic reticulum stress and aberrant mitochondrial protein expression in autophagy-deficient skeletal and cardiac muscles...
August 11, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28801645/chronic-intermittent-hypobaric-hypoxia-improves-cardiac-function-through-inhibition-of-endoplasmic-reticulum-stress
#11
Fang Yuan, Li Zhang, Yan-Qing Li, Xu Teng, Si-Yu Tian, Xiao-Ran Wang, Yi Zhang
We investigated the role of endoplasmic reticulum stress (ERS) in chronic intermittent hypobaric hypoxia (CIHH)-induced cardiac protection. Adult male Sprague-Dawley rats were exposed to CIHH treatment simulating 5000 m altitude for 28 days, 6 hours per day. The heart was isolated and perfused with Langendorff apparatus and subjected to 30-min ischemia followed by 60-min reperfusion. Cardiac function, infarct size, and lactate dehydrogenase (LDH) activity were assessed. Expression of ERS molecular chaperones (GRP78, CHOP and caspase-12) was assayed by western blot analysis...
August 11, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28794819/upregulation-of-autophagy-genes-and-the-unfolded-protein-response-in-human-heart-failure
#12
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/28768233/identification-of-transcriptome-signature-for-myocardial-reductive-stress
#13
Justin M Quiles, Madhusudhanan Narasimhan, Timothy Mosbruger, Gobinath Shanmugam, David Crossman, Namakkal S Rajasekaran
The nuclear factor erythroid 2 like 2 (Nfe2l2/Nrf2) is a master regulator of antioxidant gene transcription. We recently identified that constitutive activation of Nrf2 (CaNrf2) caused reductive stress (RS) in the myocardium. Here we investigate how chronic Nrf2 activation alters myocardial mRNA transcriptome in the hearts of CaNrf2 transgenic (TG-low and TG-high) mice using an unbiased integrated systems approach and next generation RNA sequencing followed by qRT-PCR methods. A total of 246 and 1031 differentially expressed genes (DEGs) were identified in the heart of TGL and TGH in relation to NTG littermates at ~ 6 months of age...
October 2017: Redox Biology
https://www.readbyqxmd.com/read/28767701/cardiac-directed-expression-of-a-catalytically-inactive-adenylyl-cyclase-6-protects-the-heart-from-sustained-%C3%AE-adrenergic-stimulation
#14
Mei Hua Gao, N Chin Lai, Dimosthenis Giamouridis, Young Chul Kim, Tracy Guo, H Kirk Hammond
OBJECTIVES: Increased expression of adenylyl cyclase type 6 (AC6) has beneficial effects on the heart through cyclic adenosine monophosphate (cAMP)-dependent and cAMP-independent pathways. We previously generated a catalytically inactive mutant of AC6 (AC6mut) that has an attenuated response to β-adrenergic receptor stimulation, and, consequently, exhibits reduced myocardial cAMP generation. In the current study we test the hypothesis that cardiac-directed expression of AC6mut would protect the heart from sustained β-adrenergic receptor stimulation, a condition frequently encountered in patients with heart failure...
2017: PloS One
https://www.readbyqxmd.com/read/28757580/role-of-mitochondria-and-endoplasmic-reticulum-in-taurine-deficiency-mediated-apoptosis
#15
Chian Ju Jong, Takashi Ito, Howard Prentice, Jang-Yen Wu, Stephen W Schaffer
Taurine is a ubiquitous sulfur-containing amino acid found in high concentration in most tissues. Because of its involvement in fundamental physiological functions, such as regulating respiratory chain activity, modulating cation transport, controlling inflammation, altering protein phosphorylation and prolonging lifespan, taurine is an important nutrient whose deficiency leads to severe pathology and cell death. However, the mechanism by which taurine deficiency causes cell death is inadequately understood...
July 25, 2017: Nutrients
https://www.readbyqxmd.com/read/28753907/shikonin-ameliorates-isoproterenol-iso-induced-myocardial-damage-through-suppressing-fibrosis-inflammation-apoptosis-and-er-stress
#16
Jun Yang, Zhao Wang, Dong-Lin Chen
Shikonin, isolated from the roots of herbal plant Lithospermum erythrorhizon, is a naphthoquinone. It has been reported to exert beneficial anti-inflammatory effects and anti-oxidant properties in various diseases. Isoproterenol (ISO) has been widely used to establish cardiac injury in vivo and in vitro. However, shikonin function in ISO-induced cardiac injury remains uncertain. In our study, we attempted to investigate the efficiency and possible molecular mechanism of shikonin in cardiac injury treatment induced by ISO...
September 2017: Biomedicine & Pharmacotherapy, Biomédecine & Pharmacothérapie
https://www.readbyqxmd.com/read/28748322/schisandrin-b-ameliorates-myocardial-ischemia-reperfusion-injury-through-attenuation-of-endoplasmic-reticulum-stress-induced-apoptosis
#17
Wei Zhang, Zhiqing Sun, Fanhua Meng
Schisandrin B (Sch B), an active composition isolated from the fruit of Schisandra chinensis, has been proved to possess antiinflammatory, antioxidant and anti-endoplasmic reticulum (ER) stress effects in many rodent tissues. However, the exact mechanism of cardioprotective effect of Sch B still needs more study. Here, we detected the effects of Sch B on myocardial ischemia/reperfusion (I/R) injury rats. I/R injury model in this study was established by left anterior descending coronary artery ligation for 40 min followed by 1 h of reperfusion...
July 26, 2017: Inflammation
https://www.readbyqxmd.com/read/28743963/a-non-canonical-pathway-regulates-er-stress-signaling-and-blocks-er-stress-induced-apoptosis-and-heart-failure
#18
Yufeng Yao, Qiulun Lu, Zhenkun Hu, Yubin Yu, Qiuyun Chen, Qing K Wang
Endoplasmic reticulum stress is an evolutionarily conserved cell stress response associated with numerous diseases, including cardiac hypertrophy and heart failure. The major endoplasmic reticulum stress signaling pathway causing cardiac hypertrophy involves endoplasmic reticulum stress sensor PERK (protein kinase-like kinase) and eIF2α-ATF4-CHOP signaling. Here, we describe a non-canonical, AGGF1-mediated regulatory system for endoplasmic reticulum stress signaling associated with increased p-eIF2α and ATF4 and decreased sXBP1 and CHOP...
July 25, 2017: Nature Communications
https://www.readbyqxmd.com/read/28734932/a-pyridone-derivative-activates-serca2a-by-attenuating-the-inhibitory-effect-of-phospholamban
#19
Manami Kaneko, Hisato Yamamoto, Hiroki Sakai, Yusuke Kamada, Toshiki Tanaka, Shuji Fujiwara, Synsuke Yamamoto, Hiroki Takahagi, Hideyuki Igawa, Shizuo Kasai, Masakuni Noda, Makoto Inui, Tomoyuki Nishimoto
The cardiac sarco/endoplasmic reticulum Ca(2+)-dependent ATPase 2a (SERCA2a) plays a central role in Ca(2+) handling within cardiomyocytes and is negatively regulated by phospholamban (PLN), a sarcoplasmic reticulum (SR) membrane protein. The activation of SERCA2a, which has been reported to improve cardiac dysfunction in heart failure, is a potential therapeutic approach for heart failure. Therefore, we developed a novel small molecule, compound A and characterized it both in vitro and in vivo. Compound A activated the Ca(2+)-dependent ATPase activity of cardiac SR vesicles but not that of skeletal muscle SR vesicles that lack PLN...
July 19, 2017: European Journal of Pharmacology
https://www.readbyqxmd.com/read/28713984/downregulation-of-microrna%C3%A2-199a%C3%A2-5p-protects-cardiomyocytes-in-cyanotic-congenital-heart-disease-by-attenuating-endoplasmic-reticulum-stress
#20
Yang Zhou, Wei-Kun Jia, Zhao Jian, Liang Zhao, Chen-Cheng Liu, Yong Wang, Ying-Bin Xiao
Chronic hypoxia is a key pathological change in patients with cyanotic congenital heart defect (CCHD). It has been demonstrated that enhanced myocardial unfolded protein response (UPR) increases the capacity to buffer endoplasmic reticulum (ER) stress and to avoid subsequent apoptosis caused by the hypoxia that underlies CCHD. The present study was performed to determine the regulatory role of microRNAs (miRNAs) in this cytoprotective UPR process. The results revealed that miR‑199a‑5p was markedly downregulated in the cardiac tissue of patients with CCHD and in human myocardial cells cultured in hypoxic conditions...
September 2017: Molecular Medicine Reports
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