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Transverse aortic constriction

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https://www.readbyqxmd.com/read/27920122/microrna-33-controls-adaptive-fibrotic-response-in-the-remodeling-heart-by-preserving-lipid-raft-cholesterol
#1
Masataka Nishiga, Takahiro Horie, Yasuhide Kuwabara, Kazuya Nagao, Osamu Baba, Tetsushi Nakao, Tomohiro Nishino, Daihiko Hakuno, Yasuhiro Nakashima, Hitoo Nishi, Fumiko Nakazeki, Yuya Ide, Satoshi Koyama, Masahiro Kimura, Ritsuko Hanada, Tomoyuki Nakamura, Tsukasa Inada, Koji Hasegawa, Simon J Conway, Toru Kita, Takeshi Kimura, Koh Ono
RATIONALE: Heart failure (HF) and atherosclerosis share the underlying mechanisms of chronic inflammation followed by fibrosis. A highly conserved microRNA (miR), miR-33 is considered as a potential therapeutic target for atherosclerosis because it regulates lipid metabolism and inflammation. However, the role of miR-33 in HF remains to be elucidated. OBJECTIVE: To clarify the role of miR-33 involved in HF. METHODS AND RESULTS: We first investigated the expression levels of miR-33a/b in human cardiac tissue samples with dilated cardiomyopathy...
December 5, 2016: Circulation Research
https://www.readbyqxmd.com/read/27915044/a-novel-aldosterone-synthase-inhibitor-ameliorates-mortality-in-pressure-overload-mice-with-heart-failure
#2
Shinji Furuzono, Masaki Meguro, Satoru Miyauchi, Shinichi Inoue, Tsuyoshi Homma, Keisuke Yamada, Yoh-Ichi Tagawa, Futoshi Nara, Takahiro Nagayama
It has been elucidated that mineralocorticoid receptor antagonists reduce mortality in patients with congestive heart failure and post-acute myocardial infarction. A direct inhibition of aldosterone synthase (CYP11B2) is also expected to have therapeutic benefits equal in quality to mineralocorticoid receptor antagonists in terms of reducing mineralocorticoid receptor signaling. Therefore, we have screened our chemical libraries and identified a novel and potent aldosterone synthase inhibitor, 2,2,2-trifluoro-1-{4-[(4-fluorophenyl)amino]pyrimidin-5-y}-1-[1-(methylsulfonyl)piperidin-4-yl]ethanol (compound 1), by lead optimization...
November 30, 2016: European Journal of Pharmacology
https://www.readbyqxmd.com/read/27893819/salvianolic-acid-b-alleviates-heart-failure-by-inactivating-erk1-2-gata4-signaling-pathway-after-pressure-overload-in-mice
#3
Juan Yu, Renshan Chen, Yafang Tan, Jiashin Wu, Jianyong Qi, Minzhou Zhang, Weiwang Gu
BACKGROUND: Heart failure(HF) is a dangerous disease that affects millions of patients. Radix Salvia is widely used in Chinese clinics to treat heart diseases. Salvianolic acid B(SalB) is the major active component of Radix Salvia. This study investigated the mechanisms of action and effects of SalB on HF in an experimental mouse model of HF. METHODS: We created a mouse model of HF by inducing pressure overload with transverse aortic constriction(TAC) surgery for 2 weeks and compared among 4 study groups: SHAM group (n = 10), TAC group (n = 9), TAC+MET group (metprolol, positive drug treatment, n = 9) and TAC+SalB group (SalB, 240 mg•kg-1•day-1, n = 9)...
2016: PloS One
https://www.readbyqxmd.com/read/27889753/renal-denervation-attenuates-multi-organ-fibrosis-and-improves-vascular-remodeling-in-rats-with-transverse-aortic-constriction-induced-cardiomyopathy
#4
Kai Wang, Dasheng Lu, Bin Zhang, Shengchan Wang, Qian Liu, Qi Zhang, Jie Geng, Qijun Shan
BACKGROUND/AIMS: To investigate the effects of renal denervation (RDN) on multi-organ fibrosis and vascular remodeling in cardiomyopathy. METHODS: Thirty-six male Sprague-Dawley rats underwent transverse aortic constriction (TAC). Five weeks later, 28 surviving TAC rats were randomly assigned to three groups: (1) RDN, (2) Sham, (3) Carvedilol. Six male Sham TAC rats served as the Control. Ten weeks after TAC, samples were collected. RESULTS: TAC rats showed an increased diastolic interventricular septal thickness at week 5...
November 25, 2016: Cellular Physiology and Biochemistry
https://www.readbyqxmd.com/read/27886143/neonatal-diesel-exhaust-particulate-exposure-does-not-predispose-mice-to-adult-cardiac-hypertrophy-or-heart-failure
#5
Yonggang Liu, Chad S Weldy, Michael T Chin
Background: We have previously reported that in utero and early life exposure to diesel exhaust particulates predisposes mice to adult heart failure, and that in utero exposure alone is sufficient to confer this predisposition. This follow up study addresses whether neonatal exposure alone can also confer this predisposition. Methods: Newborn male C57BL/6 mice were exposed to diesel exhaust (DE) particulates immediately after birth until weaning at 21 days of age, whereupon they were transferred to filtered air (FA) conditions...
November 24, 2016: International Journal of Environmental Research and Public Health
https://www.readbyqxmd.com/read/27876880/overexpression-of-serpine2-protease-nexin-1-contribute-to-pathological-cardiac-fibrosis-via-increasing-collagen-deposition
#6
Xuelian Li, Dandan Zhao, Zhenfeng Guo, Tianshi Li, Muge Qili, Bozhi Xu, Ming Qian, Haihai Liang, Xiaoqiang E, Samuel Chege Gitau, Lu Wang, Longtao Huangfu, Qiuxia Wu, Chaoqian Xu, Hongli Shan
Although increases in cardiovascular load (pressure overload) are known to elicit ventricular remodeling including cardiomyocyte hypertrophy and interstitial fibrosis, the molecular mechanisms of pressure overload or AngII -induced cardiac interstitial fibrosis remain elusive. In this study, serpinE2/protease nexin-1 was over-expressed in a cardiac fibrosis model induced by pressure-overloaded via transverse aortic constriction (TAC) in mouse. Knockdown of serpinE2 attenuates cardiac fibrosis in a mouse model of TAC...
November 23, 2016: Scientific Reports
https://www.readbyqxmd.com/read/27876471/cobalamin-and-folate-protect-mitochondrial-and-contractile-functions-in-a-murine-model-of-cardiac-pressure-overload
#7
Jérôme Piquereau, Maryline Moulin, Giada Zurlo, Philippe Mateo, Mélanie Gressette, Jean-Louis Paul, Christophe Lemaire, Renée Ventura-Clapier, Vladimir Veksler, Anne Garnier
PGC-1α, a key regulator of energy metabolism, seems to be a relevant therapeutic target to rectify the energy deficit observed in heart failure (HF). Since our previous work has shown positive effects of cobalamin (Cb) on PGC-1α cascade, we investigate the protective role of Cb in pressure overload-induced myocardial dysfunction. Mice were fed with normal diet (ND) or with Cb and folate supplemented diet (SD) 3weeks before and 4weeks after transverse aortic constriction (TAC). At the end, left ventricle hypertrophy and drop of ejection fraction were significantly lower in SD mice than in ND mice...
November 19, 2016: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/27836671/glycine-prevents-pressure-overload-induced-cardiac-hypertrophy-mediated-by-glycine-receptor
#8
Yan Lu, Xudong Zhu, Jinjie Li, Ru Fang, Zhuoyun Wang, Jing Zhang, Kexue Li, Xiaoyu Li, Hui Bai, Qing Yang, Jingjing Ben, Hanwen Zhang, Qi Chen
As a major amino acid, glycine has multiple functions in metabolism, growth, immunity, cytoprotection, and survival. The aim of this study was to determine the effects of glycine on pathologic cardiac hypertrophy and the mechanism underlying it. Pre-treatment with glycine significantly attenuated murine cardiac hypertrophy induced by transverse aortic constriction or by administration of angiotensin II (Ang II). This action was associated with a suppressive extracellular signal-regulated kinase 1/2 phosphorylation in myocardium...
November 9, 2016: Biochemical Pharmacology
https://www.readbyqxmd.com/read/27829660/periodontitis-and-myocardial-hypertrophy
#9
REVIEW
Jun-Ichi Suzuki, Hiroki Sato, Makoto Kaneko, Asuka Yoshida, Norio Aoyama, Shouta Akimoto, Kouji Wakayama, Hidetoshi Kumagai, Yuichi Ikeda, Hiroshi Akazawa, Yuichi Izumi, Mitsuaki Isobe, Issei Komuro
There is a deep relationship between cardiovascular disease and periodontitis. It has been reported that myocardial hypertrophy may be affected by periodontitis in clinical settings. Although these clinical observations had some study limitations, they strongly suggest a direct association between severity of periodontitis and left ventricular hypertrophy. However, the detailed mechanisms between myocardial hypertrophy and periodontitis have not yet been elucidated. Recently, we demonstrated that periodontal bacteria infection is closely related to myocardial hypertrophy...
November 10, 2016: Hypertension Research: Official Journal of the Japanese Society of Hypertension
https://www.readbyqxmd.com/read/27829645/an-ep4-receptor-agonist-inhibits-cardiac-fibrosis-through-activation-of-pka-signaling-in-hypertrophied-heart
#10
Qi Wang, Toru Oka, Kiyoshi Yamagami, Jong-Kook Lee, Hiroshi Akazawa, Atsuhiko T Naito, Taku Yasui, Takamaru Ishizu, Yoshikazu Nakaoka, Yasushi Sakata, Issei Komuro
Cardiac fibrosis is a pathological feature of myocardium of failing heart and plays causative roles in arrhythmia and cardiac dysfunction, but its regulatory mechanisms remain largely elusive. In this study, we investigated the effects of the novel EP4 receptor agonist ONO-0260164 on cardiac fibrosis in hypertrophied heart and explored the regulatory mechanisms in cardiac fibroblasts.In a mouse model of cardiac hypertrophy generated by transverse aortic constriction (TAC), ONO-0260164 treatment significantly prevented systolic dysfunction and progression of myocardial fibrosis at 5 weeks after TAC...
November 9, 2016: International Heart Journal
https://www.readbyqxmd.com/read/27821723/c1q-tnf-related-protein-9-promotes-cardiac-hypertrophy-and-failure
#11
Mahesh Appari, Astrid Breitbart, Florian Brandes, Malgorzata Szaroszyk, Natali Froese, Mortimer Korf-Klingebiel, Mona Malek Mohammadi, Andrea Grund, Gesine M Scharf, Honghui Wang, Carolin Zwadlo, Daniela Fraccarollo, Ulrike Schrameck, Mona Nemer, William Wong, Hugo A Katus, Kai C Wollert, Oliver J Müller, Johann Bauersachs, Joerg Heineke
RATIONALE: Myocardial endothelial cells promote cardiomyocyte hypertrophy, possibly through the release of growth factors. The identity of these factors, however, remains largely unknown, and we hypothesized here that the secreted C1q-TNF-related protein-9 (CTRP9) might act as endothelial derived protein to modulate heart remodeling in response to pressure overload. OBJECTIVE: To examine the source of cardiac CTRP9 and its function during pressure overload. METHODS AND RESULTS: CTRP9 was mainly derived from myocardial capillary endothelial cells...
November 7, 2016: Circulation Research
https://www.readbyqxmd.com/read/27811197/phospholamban-inhibition-by-a-single-dose-of-locked-nucleic-acid-antisense-oligonucleotide-improves-cardiac-contractility-in-pressure-overload-induced-systolic-dysfunction-in-mice
#12
Hirofumi Morihara, Tsuyoshi Yamamoto, Harunori Oiwa, Kota Tonegawa, Daisuke Tsuchiyama, Ikki Kawakatsu, Masanori Obana, Makiko Maeda, Tomomi Mohri, Satoshi Obika, Yasushi Fujio, Hiroyuki Nakayama
BACKGROUND: Phospholamban (PLN) inhibition enhances calcium cycling and is a potential novel therapy for heart failure (HF). Antisense oligonucleotides (ASOs) are a promising tool for unmet medical needs. Nonviral vector use of locked nucleic acid (LNA)-modified ASOs (LNA-ASOs), which shows strong binding to target RNAs and is resistant to nuclease, is considered to have a potential for use in novel therapeutics in the next decades. Thus, the efficacy of a single-dose injection of LNA-ASO for cardiac disease needs to be elucidated...
November 2, 2016: Journal of Cardiovascular Pharmacology and Therapeutics
https://www.readbyqxmd.com/read/27796324/myocyte-specific-enhancer-factor-2c-a-novel-target-gene-of-mir-214-3p-in-suppressing-angiotensin-ii-induced-cardiomyocyte-hypertrophy
#13
Chun-Mei Tang, Fang-Zhou Liu, Jie-Ning Zhu, Yong-Heng Fu, Qiu-Xiong Lin, Chun-Yu Deng, Zhi-Qin Hu, Hui Yang, Xi-Long Zheng, Jian-Ding Cheng, Shu-Lin Wu, Zhi-Xin Shan
The role of microRNA-214-3p (miR-214-3p) in cardiac hypertrophy was not well illustrated. The present study aimed to investigate the expression and potential target of miR-214-3p in angiotensin II (Ang-II)-induced mouse cardiac hypertrophy. In mice with either Ang-II infusion or transverse aortic constriction (TAC) model, miR-214-3p expression was markedly decreased in the hypertrophic myocardium. Down-regulation of miR-214-3p was observed in the myocardium of patients with cardiac hypertrophy. Expression of miR-214-3p was upregulated in Ang-II-induced hypertrophic neonatal mouse ventricular cardiomyocytes...
October 31, 2016: Scientific Reports
https://www.readbyqxmd.com/read/27791092/pde1c-deficiency-antagonizes-pathological-cardiac-remodeling-and-dysfunction
#14
Walter E Knight, Si Chen, Yishuai Zhang, Masayoshi Oikawa, Meiping Wu, Qian Zhou, Clint L Miller, Yujun Cai, Deanne M Mickelsen, Christine Moravec, Eric M Small, Junichi Abe, Chen Yan
Cyclic nucleotide phosphodiesterase 1C (PDE1C) represents a major phosphodiesterase activity in human myocardium, but its function in the heart remains unknown. Using genetic and pharmacological approaches, we studied the expression, regulation, function, and underlying mechanisms of PDE1C in the pathogenesis of cardiac remodeling and dysfunction. PDE1C expression is up-regulated in mouse and human failing hearts and is highly expressed in cardiac myocytes but not in fibroblasts. In adult mouse cardiac myocytes, PDE1C deficiency or inhibition attenuated myocyte death and apoptosis, which was largely dependent on cyclic AMP/PKA and PI3K/AKT signaling...
October 20, 2016: Proceedings of the National Academy of Sciences of the United States of America
https://www.readbyqxmd.com/read/27789290/ablation-of-biglycan-attenuates-cardiac-hypertrophy-and-fibrosis-after-left-ventricular-pressure-overload
#15
Nadine Beetz, Carolin Rommel, Tilman Schnick, Elena Neumann, Achim Lother, Elsa Beatriz Monroy-Ordonez, Martin Zeeb, Sebastian Preissl, Ralf Gilsbach, Ariane Melchior-Becker, Bartosz Rylski, Monika Stoll, Liliana Schaefer, Friedhelm Beyersdorf, Brigitte Stiller, Lutz Hein
AIMS: Biglycan, a small leucine-rich proteoglycan, has been shown to play an important role in stabilizing fibrotic scars after experimental myocardial infarction. However, the role of biglycan in the development and regression of cardiomyocyte hypertrophy and fibrosis during cardiac pressure overload and unloading remains elusive. Thus, the aim of the present study was to assess the effect of biglycan on cardiac remodeling in a mouse model of left ventricular pressure overload and unloading...
October 24, 2016: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/27789286/effects-of-induced-na-ca-2-exchanger-overexpression-on-the-spatial-distribution-of-l-type-ca-2-channels-and-junctophilin-2-in-pressure-overloaded-hearts
#16
Yoshihiro Ujihara, Satoshi Mohri, Yuki Katanosaka
The Na(+)/Ca(2+) exchanger 1 (NCX1) is an essential Ca(2+) efflux system in cardiomyocytes. Although NCX1 is distributed throughout the sarcolemma, a subpopulation of NCX1 is localized to transverse (T)-tubules. There is growing evidence that T-tubule disorganization is a causal event that shifts the transition from hypertrophy to heart failure (HF). However, the detailed molecular mechanisms have not been clarified. Previously, we showed that induced NCX1 expression in pressure-overloaded hearts attenuates defective excitation-contraction coupling and HF progression...
October 24, 2016: Biochemical and Biophysical Research Communications
https://www.readbyqxmd.com/read/27773659/ascending-aortic-adventitial-remodeling-and-fibrosis-are-ameliorated-with-apelin-13-in-rats-after-tac-via-suppression-of-the-mirna-122-and-lgr4-%C3%AE-catenin-signaling
#17
Ran Xu, Zhen-Zhou Zhang, Lai-Jiang Chen, Hui-Min Yu, Shu-Jie Guo, Ying-Le Xu, Gavin Y Oudit, Yan Zhang, Qing Chang, Bei Song, Dong-Rui Chen, Ding-Liang Zhu, Jiu-Chang Zhong
Apelin has been proved to be a critical mediator of vascular function and homeostasis. Here, we investigated roles of Apelin in aortic remodeling and fibrosis in rats with transverse aortic constriction (TAC). Male Sprague-Dawley rats were subjected to TAC and then randomized to daily deliver Apelin-13 (50μg/kg) or angiotensin type 1 receptor (AT1) blocker Irbesartan (50mg/kg) for 4 weeks. Pressure overload resulted in myocardial hypertrophy, systolic dysfunction, aortic remodeling and adventitial fibrosis with reduced levels of Apelin in ascending aortas of rat after TAC compared with sham-operated group...
December 2016: Peptides
https://www.readbyqxmd.com/read/27771553/correction-of-impaired-calmodulin-binding-to-ryr2-as-a-novel-therapy-for-lethal-arrhythmia-in-the-pressure-overloaded-heart-failure
#18
Takayoshi Kato, Takeshi Yamamoto, Yoshihide Nakamura, Takuma Nanno, Go Fukui, Yoko Sufu, Yoriomi Hamada, Takako Maeda, Shigehiko Nishimura, Hironori Ishiguchi, Wakako Murakami, Masakazu Fukuda, Xiaojuan Xu, Akihiro Hino, Makoto Ono, Tetsuro Oda, Shinichi Okuda, Shigeki Kobayashi, Noritaka Koseki, Hiroyuki Kyushiki, Masafumi Yano
BACKGROUND: Calmodulin (CaM) is a key modulator of the channel gating function of the ryanodine receptor (RyR). OBJECTIVE: The purpose of this study was to investigate the pathogenic role of RyR-bound CaM in diastolic Ca(2+) leakage from the sarcoplasmic reticulum and arrhythmogenesis in pressure-overloaded heart failure. METHODS: Pressure overload was induced in 12-week-old mice by transverse aortic constriction (TAC) using a 27-gauge needle...
October 19, 2016: Heart Rhythm: the Official Journal of the Heart Rhythm Society
https://www.readbyqxmd.com/read/27766308/cardiac-disease-and-arrhythmogenesis-mechanistic-insights-from-mouse-models
#19
Lois Choy, Jie Ming Yeo, Vivian Tse, Shing Po Chan, Gary Tse
The mouse is the second mammalian species, after the human, in which substantial amount of the genomic information has been analyzed. With advances in transgenic technology, mutagenesis is now much easier to carry out in mice. Consequently, an increasing number of transgenic mouse systems have been generated for the study of cardiac arrhythmias in ion channelopathies and cardiomyopathies. Mouse hearts are also amenable to physical manipulation such as coronary artery ligation and transverse aortic constriction to induce heart failure, radiofrequency ablation of the AV node to model complete AV block and even implantation of a miniature pacemaker to induce cardiac dyssynchrony...
September 2016: IJC Heart & Vasculature
https://www.readbyqxmd.com/read/27760414/junctophilin-2-gene-therapy-rescues-heart-failure-by-normalizing-ryr2-mediated-ca-2-release
#20
Julia O Reynolds, Ann P Quick, Qiongling Wang, David L Beavers, Leonne E Philippen, Jordan Showell, Giselle Barreto-Torres, Donna J Thuerauf, Shirin Doroudgar, Christopher C Glembotski, Xander H T Wehrens
BACKGROUND: Junctophilin-2 (JPH2) is the primary structural protein for the coupling of transverse (T)-tubule associated cardiac L-type Ca channels and type-2 ryanodine receptors on the sarcoplasmic reticulum within junctional membrane complexes (JMCs) in cardiomyocytes. Effective signaling between these channels ensures adequate Ca-induced Ca release required for normal cardiac contractility. Disruption of JMC subcellular domains, a common feature of failing hearts, has been attributed to JPH2 downregulation...
December 15, 2016: International Journal of Cardiology
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