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stress induced cardiomyopathy

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https://www.readbyqxmd.com/read/28629836/opposite-effects-of-catalase-and-mnsod-ectopic-expression-on-stress-induced-defects-and-mortality-in-the-desmin-deficient-cardiomyopathy-model
#1
Kleopatra Rapti, Antigoni Diokmetzidou, Ismini Kloukina, Derek J Milner, Aimilia Varela, Constantinos H Davos, Yassemi Capetanaki
Oxidative stress has been linked strongly to cell death and cardiac remodeling processes, all hallmarks of heart failure. Mice deficient for desmin (des-/-), the major muscle specific intermediate filament protein, develop dilated cardiomyopathy and heart failure characterized by mitochondrial defects and cardiomyocyte death. The cellular and biochemical alterations in the hearts of these mice strongly suggest that oxidative stress is one of the mechanisms contributing to the pathogenesis of the phenotype. Recently, we showed that indeed the desmin deficient cardiomyocytes are under increased oxidative stress...
June 16, 2017: Free Radical Biology & Medicine
https://www.readbyqxmd.com/read/28624452/fortunellin-protects-against-high-fructose-induced-diabetic-heart-injury-in-mice-by-suppressing-inflammation-and-oxidative-stress-via-ampk-nrf-2-pathway-regulation
#2
Cuihua Zhao, Yuan Zhang, Hongyang Liu, Peng Li, Han Zhang, Guanchang Cheng
Inflammation and oxidative stress contribute to the progression of diabetic cardiomyopathy (DCM). The study was first designed to calculate the role of an anti-inflammatory and anti-oxidant Fortunellin (For) in high fructose-induced cardiac injury in diabetic mice. Fortunellin was found to be none of toxicity to mice and cells using various assays. High fructose was used to induce mice with diabetes. The heart histopathological changes and cardiac function were measured. Fortunellin significantly attenuated the score of histopathological alterations and alleviated heart function, accompanied with reduced inflammation and oxidative stress...
June 14, 2017: Biochemical and Biophysical Research Communications
https://www.readbyqxmd.com/read/28623080/increased-constitutive-nitric-oxide-production-by-whole-body-periodic-acceleration-ameliorates-alterations-in-cardiomyocytes-associated-with-utrophin-dystrophin-deficiency
#3
Jose R Lopez, Juan Kolster, Rui Zhang, Jose Adams
Duchenne Muscular Dystrophy (DMD) cardiomyopathy is a progressive lethal disease caused by the lack of the dystrophin protein in the heart. The most widely used animal model of DMD is the dystrophin-deficient mdx mouse; however, these mice exhibit a mild dystrophic phenotype with heart failure only late in life. In contrast, mice deficient for both dystrophin and utrophin (mdx/utrn(-/-), or dKO) can be used to model severe DMD cardiomyopathy where pathophysiological indicators of heart failure are detectable by 8-10weeks of age...
June 13, 2017: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/28608983/folic-acid-reduces-doxorubicin-induced-cardiomyopathy-by-modulating-endothelial-nitric-oxide-synthase
#4
Yanti Octavia, Georgios Kararigas, Martine de Boer, Ihsan Chrifi, Rinrada Kietadisorn, Melissa Swinnen, Hans Duimel, Fons K Verheyen, Maarten M Brandt, Daniela Fliegner, Caroline Cheng, Stefan Janssens, Dirk J Duncker, An L Moens
The use of doxorubicin (DOXO) as a chemotherapeutic drug has been hampered by cardiotoxicity leading to cardiomyopathy and heart failure. Folic acid (FA) is a modulator of endothelial nitric oxide (NO) synthase (eNOS), which in turn is an important player in diseases associated with NO insufficiency or NOS dysregulation, such as pressure overload and myocardial infarction. However, the role of FA in DOXO-induced cardiomyopathy is poorly understood. The aim of this study was to test the hypothesis that FA prevents DOXO-induced cardiomyopathy by modulating eNOS and mitochondrial structure and function...
June 13, 2017: Journal of Cellular and Molecular Medicine
https://www.readbyqxmd.com/read/28607937/contrast-media-induced-anaphylaxis-causing-a-stress-related-cardiomyopathy-post-percutaneous-coronary-intervention-case-report
#5
Rajeev Seecheran, Valmiki Seecheran, Sangeeta Persad, Sasha Lalla, Naveen Anand Seecheran
Anaphylaxis is a sudden-onset, severe hypersensitivity reaction that can be potentially fatal. It can often transition to refractory hemodynamic instability, eventually resulting in death. Stress-related cardiomyopathies (SRCs) have multifactorial etiologies, including being linked to excessive catecholamine release in periods of intense stress. This novel case report recounts a SRC caused by contrast-induced anaphylaxis within 1 hour post percutaneous coronary intervention. Both acutely life-threatening conditions may occur simultaneously and are implicated with devastating complications...
April 2017: Journal of Investigative Medicine High Impact Case Reports
https://www.readbyqxmd.com/read/28606389/etiology-of-alcoholic-cardiomyopathy-mitochondria-oxidative-stress-and-apoptosis
#6
REVIEW
Jennifer L Steiner, Charles H Lang
Putative mechanisms leading to the development of alcoholic cardiomyopathy (ACM) include the interrelated cellular processes of mitochondria metabolism, oxidative stress and apoptosis. As mitochondria fuel the constant energy demands of this continually contracting tissue, it is not surprising that alcohol-induced molecular changes in this organelle contribute to cardiac dysfunction and ACM. As the causal relationship of these processes with ACM has already been established, the primary objective of this review is to provide an update of the experimental findings to more completely understand the aforementioned mechanisms...
June 9, 2017: International Journal of Biochemistry & Cell Biology
https://www.readbyqxmd.com/read/28599831/alterations-in-cardiac-deformation-timing-of%C3%A2-contraction-and-relaxation-and-early-myocardial-fibrosis-accompany-the-apparent-recovery-of-acute-stress-induced-takotsubo-cardiomyopathy-an-end-to-the-concept-of%C3%A2-transience
#7
Konstantin Schwarz, Trevor Ahearn, Janaki Srinivasan, Christopher J Neil, Caroline Scally, Amelia Rudd, Baljit Jagpal, Michael P Frenneaux, Cristina Pislaru, John D Horowitz, Dana K Dawson
BACKGROUND: Takotsubo syndrome is an increasingly recognized cause of chest pain and occasionally of cardiogenic shock. Despite rapid improvement of the left ventricular (LV) ejection fraction, recent registry data raise concerns about long-term prognosis. The aim of this study was to test the hypothesis that restoration of normal ejection fraction after acute takotsubo syndrome is not equivalent to full functional recovery. METHODS: Fifty-two patients with takotsubo syndrome (according to the Mayo Clinic criteria plus cardiac magnetic resonance imaging to exclude myocardial infarction) and 44 healthy control subjects of the same age, gender, and cardiovascular comorbidity distribution were prospectively recruited...
June 6, 2017: Journal of the American Society of Echocardiography
https://www.readbyqxmd.com/read/28588076/pai-1-controls-cardiomyocyte-tgf-%C3%AE-and-cardiac-fibrosis
#8
Panagiotis Flevaris, Sadiya S Khan, Mesut Eren, Adam J Schuldt, Sanjiv J Shah, Daniel C Lee, Sweta Gupta, Amy Shapiro, Paul Burridge, Asish K Ghosh, Douglas E Vaughan
Background -Fibrosis is the pathologic consequence of stress-induced tissue remodeling and matrix accumulation. Increased levels of plasminogen activator inhibitor type I (PAI-1) have been shown to promote fibrosis in multiple organ systems. Paradoxically, homozygous genetic deficiency of PAI-1 is associated with spontaneous age-dependent cardiac-selective fibrosis in mice. We have identified a novel PAI-1-dependent mechanism that regulates cardiomyocyte-derived fibrogenic signals and cardiac transcriptional pathways during injury...
June 6, 2017: Circulation
https://www.readbyqxmd.com/read/28580486/the-role-of-endogenous-opioid-system-in-the-regulation-of-heart-tolerance-to-stress-induced-damage
#9
Yu B Lishmanov, S Yu Tsibul'nikov, N V Naryzhnaya, M V Korobov, L N Maslov
In Wistar rats, stress was modeled by 24-h immobilization in a supine posture and stress-induced damage to the heart was assessed by accumulation of (99m)Tc-pyrophosphate in the myocardium. The intensity of stress reaction was measured by serum levels of cortisol and insulin. Both stressinduced damage to the heart and intensity of stress reaction were examined under control conditions and in rats treated with opioid receptor antagonists naltrexone, methylnaltrexone bromide, MR2266, and ICI174.864. Activation of central μ-opioid receptors with endogenous opioids aggravated stress-induced cardiomyopathy, while stimulation of peripheral μ-opioid receptors produced a cardioprotective effect...
June 3, 2017: Bulletin of Experimental Biology and Medicine
https://www.readbyqxmd.com/read/28577159/biventricular-thrombosis-in-biventricular-stress-takotsubo-cardiomyopathy
#10
Luisa De Gennaro, Massimo Ruggiero, Sergio Musci, Francesco Tota, Domenica De Laura, Manuela Resta, Nicola Locuratolo, Francesco Santoro, Natale Daniele Brunetti, Pasquale Caldarola
Endo-ventricular thrombosis represents a possible clinical complication of stress(takotsubo)-cardiomyopathy (SC). Depressed ventricular systolic ventricular function, localized left ventricular (LV) dyskinesis, but also an increased pro-thrombotic state induced by catecholamine surge may facilitate the occurrence of endovascular thrombosis in SC. SC, however, may also present as right ventricular (RV) dysfunction or even as biventricular ballooning. Ventricular thrombosis may therefore theoretically occur in either ventricles or both...
June 2, 2017: Journal of Thrombosis and Thrombolysis
https://www.readbyqxmd.com/read/28559425/fgf21-ameliorates-diabetic-cardiomyopathy-by-activating-the-ampk-paraoxonase-1-signaling-axis-in-mice
#11
Fan Wu, Baile Wang, Saisai Zhang, Lihua Shi, Yanfang Wang, Rongrong Xiong, Xuebo Pan, Fanghua Gong, Xiaokun Li, Zhuofeng Lin
Aims: The aim in present study is to explore the molecular mechanism of FGF21 against diabetic cardiomyopathy. Materials and methods: FGF21 deficient mice and wild type littermates were used to induce diabetic mice by treatment with streptozotocin/high-fat diet (STZ/HFD), and then evaluated the difference of diabetic cardiomyopathy between two types of mice. Otherwise, primary cultured cardiomyocytes were also used to explore the potential molecular mechanism of FGF21 against high glucose-induced cardiomyocyte injuries...
May 30, 2017: Clinical Science (1979-)
https://www.readbyqxmd.com/read/28550180/a-novel-de-novo-mutation-in-prkag2-gene-infantile-onset-phenotype-and-signaling-pathway-involved
#12
Yanchun Xu, Alex Gray, David Grahame Hardie, Alper Uzun, Sunil Shaw, James F Padbury, Chanika Phornphutkul, Yi-Tang Tseng
PRKAG2 encodes the γ2-subunit isoform of the 5' AMP-activated protein kinase (AMPK), a heterotrimeric enzyme with major roles in regulation of energy metabolism in response to cellular stress. Mutations in PRKAG2 have been implicated in a unique hypertrophic cardiomyopathy (HCM) characterized by cardiac glycogen overload, ventricular preexcitation and hypertrophy. We identified a novel, de novo PRKAG2 mutation (K475E) in a neonate with prenatal onset of HCM. We aimed to investigate the cellular impact, signaling pathways involved and therapeutic options for K475E mutation using cells stably expressing human wild type (WT) or the K475E mutant...
May 26, 2017: American Journal of Physiology. Heart and Circulatory Physiology
https://www.readbyqxmd.com/read/28546113/stretch-activated-trpv2-channels-role-in-mediating-cardiopathies
#13
REVIEW
Elizabeth Aguettaz, Patrick Bois, Christian Cognard, Stéphane Sebille
Transient receptor potential vanilloid type 2, TRPV2, is a calcium-permeable cation channel belonging to the TRPV channel family. Although this channel has been first characterized as a noxious heat sensor, its mechanosensor property recently gained importance in various physiological functions. TRPV2 has been described as a stretch-mediated channel and a regulator of calcium homeostasis in several cell types and has been shown to be involved in the stretch-dependent responses in cardiomyocytes. Hence, several studies in the last years support the idea that TRPV2 play a key role in the function and structure of the heart, being involved in the cardiac compensatory mechanisms in response to pathologic or exercise-induced stress...
May 22, 2017: Progress in Biophysics and Molecular Biology
https://www.readbyqxmd.com/read/28542596/progressive-mitochondrial-protein-lysine-acetylation-and-heart-failure-in-a-model-of-friedreich-s-ataxia-cardiomyopathy
#14
Amanda R Stram, Gregory R Wagner, Brian D Fogler, P Melanie Pride, Matthew D Hirschey, R Mark Payne
INTRODUCTION: The childhood heart disease of Friedreich's Ataxia (FRDA) is characterized by hypertrophy and failure. It is caused by loss of frataxin (FXN), a mitochondrial protein involved in energy homeostasis. FRDA model hearts have increased mitochondrial protein acetylation and impaired sirtuin 3 (SIRT3) deacetylase activity. Protein acetylation is an important regulator of cardiac metabolism and loss of SIRT3 increases susceptibility of the heart to stress-induced cardiac hypertrophy and ischemic injury...
2017: PloS One
https://www.readbyqxmd.com/read/28533752/protocatechuic-acid-a-phenolic-from-sansevieria-roxburghiana-leaves-suppresses-diabetic-cardiomyopathy-via-stimulating-glucose-metabolism-ameliorating-oxidative-stress-and-inhibiting-inflammation
#15
Niloy Bhattacharjee, Tarun K Dua, Ritu Khanra, Swarnalata Joardar, Ashis Nandy, Achintya Saha, Vincenzo De Feo, Saikat Dewanjee
Persistent hyperglycemia, impairment of redox status and establishment of inflammatory pathophysiology integrally play important role in the pathogenesis of diabetic cardiomyopathy (DC). Present study examined the therapeutic potential of protocatechuic acid isolated from the Sansevieria roxburghiana rhizomes against DC employing rodent model of type 2 diabetes (T2D). T2D was induced by high fat diet + a low-single dose of streptozotocin (35 mg/kg, i.p.). T2D rats exhibited significantly (p < 0.01) high fasting blood glucose level...
2017: Frontiers in Pharmacology
https://www.readbyqxmd.com/read/28533215/inhibition-of-hdac3-prevents-diabetic-cardiomyopathy-in-ove26-mice-via-epigenetic-regulation-of-dusp5-erk1-2-pathway
#16
Zheng Xu, Qian Tong, Zhiguo Zhang, Shudong Wang, Yang Zheng, Qiuju Liu, Lingbo Qian, Shao-Yu Chen, Jian Sun, Lu Cai
Inhibition of total histone deacetylases (HDACs) was phenomenally associated with the prevention of diabetic cardiomyopathy (DCM). However, which specific HDAC plays the key role in DCM remains unclear. The present study was designed to determine whether DCM can be prevented by specific inhibition of HDAC3 and to elucidate the mechanisms by which inhibition of HDAC3 prevent DCM. Type 1 diabetes OVE26 and age-matched wild-type mice were given the selective HDAC3 inhibitor RGFP966 or vehicle for 3 months. These mice were then sacrificed immediately or 3 months later for cardiac function and pathological examination...
May 22, 2017: Clinical Science (1979-)
https://www.readbyqxmd.com/read/28530215/takotsubo-cardiomyopathy-after-intravenous-epinephrine-administration-following-cardiac-arrest-provoked-by-pneumoperitoneum-a-case-report
#17
Waldemar Elikowski, Malgorzata Małek-Elikowska, Jacek Karoń, Maria Mrozińska, Alina Baszko, Karolina Horbacka
In stress-induced takotsubo cardiomyopathy (TC) high levels of catecholamines, including epinephrine, may be detected in blood. On the other hand, administration of exogenous epinephrine may occasionally result in TC. A CASE REPORT: The authors describe a case of a 58-year-old, otherwise healthy female, with TC which occurred after intravenous injection of 1 mg of epinephrine against cardiac arrest provoked by pneumoperitoneum performed before planned laparoscopic cholecystectomy. She was admitted 3 days earlier due to biliary colic following a dietary mistake...
April 21, 2017: Polski Merkuriusz Lekarski: Organ Polskiego Towarzystwa Lekarskiego
https://www.readbyqxmd.com/read/28526246/impaired-mitophagy-facilitates-mitochondrial-damage-in-danon-disease
#18
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/28524367/transplantation-of-human-villous-trophoblasts-preserves-cardiac-function-in-mice-with-acute-myocardial-infarction
#19
Zegen Wang, Ningzheng Dong, Yayan Niu, Zhiwei Zhang, Ce Zhang, Meng Liu, Tiantian Zhou, Qingyu Wu, Ke Cheng
Over the past decade, cell therapies have provided promising strategies for the treatment of ischaemic cardiomyopathy. Particularly, the beneficial effects of stem cells, including bone marrow stem cells (BMSCs), endothelial progenitor cells (EPCs), mesenchymal stem cells (MSCs), embryonic stem cells (ESCs), and induced pluripotent stem cells (iPSCs), have been demonstrated by substantial preclinical and clinical studies. Nevertheless stem cell therapy is not always safe and effective. Hence, there is an urgent need for alternative sources of cells to promote cardiac regeneration...
May 19, 2017: Journal of Cellular and Molecular Medicine
https://www.readbyqxmd.com/read/28522833/parkin-regulation-of-chop-modulates-susceptibility-to-cardiac-endoplasmic-reticulum-stress
#20
Kim Han, Shahin Hassanzadeh, Komudi Singh, Sara Menazza, Tiffany T Nguyen, Mark V Stevens, An Nguyen, Hong San, Stasia A Anderson, Yongshun Lin, Jizhong Zou, Elizabeth Murphy, Michael N Sack
The regulatory control of cardiac endoplasmic reticulum (ER) stress is incompletely characterized. As ER stress signaling upregulates the E3-ubiquitin ligase Parkin, we investigated the role of Parkin in cardiac ER stress. Parkin knockout mice exposed to aortic constriction-induced cardiac pressure-overload or in response to systemic tunicamycin (TM) developed adverse ventricular remodeling with excessive levels of the ER regulatory C/EBP homologous protein CHOP. CHOP was identified as a Parkin substrate and its turnover was Parkin-dose and proteasome-dependent...
May 18, 2017: Scientific Reports
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