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Transverse aortic constriction

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https://www.readbyqxmd.com/read/28316061/loss-of-dystrophin-is-associated-with-increased-myocardial-stiffness-in-a-model-of-left-ventricular-hypertrophy
#1
Martín Donato, Bruno Buchholz, Celina Morales, Laura Valdez, Tamara Zaobornyj, Sergio Baratta, Diamela T Paez, Mirian Matoso, Guillermo Vaccarino, Demian Chejtman, Oscar Agüero, Juan Telayna, José Navia, Alejandro Hita, Alberto Boveris, Ricardo J Gelpi
Transition from compensated to decompensated left ventricular hypertrophy (LVH) is accompanied by functional and structural changes. Here, the aim was to evaluate dystrophin expression in murine models and human subjects with LVH by transverse aortic constriction (TAC) and aortic stenosis (AS), respectively. We determined whether doxycycline (Doxy) prevented dystrophin expression and myocardial stiffness in mice. Additionally, ventricular function recovery was evaluated in patients 1 year after surgery. Mice were subjected to TAC and monitored for 3 weeks...
March 18, 2017: Molecular and Cellular Biochemistry
https://www.readbyqxmd.com/read/28300638/astaxanthin-attenuated-pressure-overload-induced-cardiac-dysfunction-and-myocardial-fibrosis-partially-by-activating-sirt1
#2
Jun Zhang, Quan-Zhen Wang, Shao-Hua Zhao, Xiang Ji, Jie Qiu, Jian Wang, Yi Zhou, Qian Cai, Jie Zhang, Hai-Qing Gao
BACKGROUND: Myocardial fibrosis contributes to cardiac dysfunction. Astaxanthin (AST), a member of the carotenoid family, is a well-known antioxidant, but its effect on and underlying mechanisms in myocardial fibrosis are poorly understood. METHODS: In vivo, myocardial fibrosis and cardiac dysfunction were induced using transverse aortic constriction (TAC). AST was administered to mice for 12weeks post-surgery. In vitro, transforming growth factor β1 (TGF-β1) was used to stimulate human cardiac fibroblasts (HCFs)...
March 12, 2017: Biochimica et Biophysica Acta
https://www.readbyqxmd.com/read/28299467/cardiomyocyte-ogt-limits-ventricular-dysfunction-in-mice-following-pressure-overload-without-affecting-hypertrophy
#3
Sujith Dassanayaka, Robert E Brainard, Lewis J Watson, Bethany W Long, Kenneth R Brittian, Angelica M DeMartino, Allison L Aird, Anna M Gumpert, Timothy N Audam, Peter J Kilfoil, Senthilkumar Muthusamy, Tariq Hamid, Sumanth D Prabhu, Steven P Jones
The myocardial response to pressure overload involves coordination of multiple transcriptional, posttranscriptional, and metabolic cues. The previous studies show that one such metabolic cue, O-GlcNAc, is elevated in the pressure-overloaded heart, and the increase in O-GlcNAcylation is required for cardiomyocyte hypertrophy in vitro. Yet, it is not clear whether and how O-GlcNAcylation participates in the hypertrophic response in vivo. Here, we addressed this question using patient samples and a preclinical model of heart failure...
May 2017: Basic Research in Cardiology
https://www.readbyqxmd.com/read/28286226/microrna-297-promotes-cardiomyocyte-hypertrophy-via-targeting-sigma-1-receptor
#4
Qinxue Bao, Mingyue Zhao, Li Chen, Yu Wang, Siyuan Wu, Wenchao Wu, Xiaojing Liu
AIMS: Sigma-1 receptor (Sig-1R) is a ligand-regulated endoplasmic reticulum (ER) chaperone involved in cardiac hypertrophy, but it is not known whether Sig-1R is regulated by microRNAs (miRNAs). According to bioinformatic analysis, miR-297 was suggested as a potential target miRNA for Sig-1R. Therefore, we verified whether miR-297 could target Sig-1R and investigated the possible mechanisms underlying the role of miR-297 in cardiac hypertrophy. MAIN METHODS: Bioinformatic analysis combined with laboratory experiments, including quantitative RT-PCR, Western blotting, and luciferase assay, were performed to identify the target miRNA of Sig-1R...
March 10, 2017: Life Sciences
https://www.readbyqxmd.com/read/28223222/disrupting-the-key-circadian-regulator-clock-leads-to-age-dependent-cardiovascular-disease
#5
Faisal J Alibhai, Jonathan LaMarre, Cristine J Reitz, Elena V Tsimakouridze, Jeffrey T Kroetsch, Steffen-Sebastian Bolz, Alex Shulman, Samantha Steinberg, Thomas P Burris, Gavin Y Oudit, Tami A Martino
The circadian mechanism underlies daily rhythms in cardiovascular physiology and rhythm disruption is a major risk factor for heart disease and worse outcomes. However, the role of circadian rhythms is generally clinically unappreciated. Clock is a core component of the circadian mechanism and here we examine the role of Clock as a vital determinant of cardiac physiology and pathophysiology in aging. Clock(Δ19/Δ19) mice develop age-dependent increases in heart weight, hypertrophy, dilation, impaired contractility, and reduced myogenic responsiveness...
February 20, 2017: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/28214892/baicalin-attenuates-cardiac-dysfunction-and-myocardial-remodeling-in-a-chronic-pressure-overload-mice-model
#6
Yanqing Zhang, Pingping Liao, Meng'en Zhu, Wei Li, Dan Hu, Siming Guan, Long Chen
BACKGROUND/AIMS: Baicalin has been shown to be effective for various animal models of cardiovascular diseases, such as pulmonary hypertension, atherosclerosis and myocardial ischaemic injury. However, whether baicalin plays a role in cardiac hypertrophy remains unknown. Here we investigated the protective effects of baicalin on cardiac hypertrophy induced by pressure overload and explored the potential mechanisms involved. METHODS: C57BL/6J-mice were treated with baicalin or vehicle following transverse aortic constriction or Sham surgery for up to 8 weeks, and at different time points, cardiac function and heart size measurement and histological and biochemical examination were performed...
February 16, 2017: Cellular Physiology and Biochemistry
https://www.readbyqxmd.com/read/28205629/mechanisms-of-chinese-medicine-xinmailong-s-protection-against-heart-failure-in-pressure-overloaded-mice-and-cultured-cardiomyocytes
#7
Jianyong Qi, Juan Yu, Yafang Tan, Renshan Chen, Wen Xu, Yanfen Chen, Jun Lu, Qin Liu, Jiashin Wu, Weiwang Gu, Minzhou Zhang
Patients with heart failure (HF) have high mortality and mobility. Xinmailong (XML) injection, a Chinese Medicine, is clinically effective in treating HF. However, the mechanism of XML's effectiveness on HF was unclear, and thus, was the target of the present study. We created a mouse model of pressure-overload-induced HF with transverse aortic constriction (TAC) surgery and compared among 4 study groups: SHAM (n = 10), TAC (n = 12), MET (metoprolol, positive drug treatment, n = 7) and XML (XML treatment, n = 14)...
February 16, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28202417/triptolide-attenuates-pressure-overload-induced-myocardial-remodeling-in-mice-via-the-inhibition-of-nlrp3-inflammasome-expression
#8
Rujun Li, Kuiying Lu, Yao Wang, Mingxing Chen, Fengyu Zhang, Hui Shen, Deshan Yao, Kaizheng Gong, Zhengang Zhang
Triptolide is the predominant active component of the Chinese herb Tripterygium wilfordii Hook F (TwHF) that has been widely used to treat several chronic inflammatory diseases due to its immunosuppressive, anti-inflammatory, and anti-proliferative properties. In the present study, we elucidated the cardioprotective effects of triptolide against cardiac dysfunction and myocardial remodeling in chronic pressure-overloaded hearts. Furthermore, the potential mechanisms of triptolide were investigated. For this purpose, C57/BL6 mice were anesthetized and subjected to transverse aortic constriction (TAC) or sham operation...
March 25, 2017: Biochemical and Biophysical Research Communications
https://www.readbyqxmd.com/read/28163023/a-novel-urotensin-ii-receptor-antagonist-kr-36996-improved-cardiac-function-and-attenuated-cardiac-hypertrophy-in-experimental-heart-failure
#9
Kwang-Seok Oh, Jeong Hyun Lee, Kyu Yang Yi, Chae Jo Lim, Byung Kil Park, Ho Won Seo, Byung Ho Lee
Urotensin II and its receptor are thought to be involved in various cardiovascular diseases such as heart failure, pulmonary hypertension and atherosclerosis. Since the regulation of the urotensin II/urotensin II receptor offers a great potential for therapeutic strategies related to the treatment of cardiovascular diseases, the study of selective and potent antagonists for urotensin II receptor is more fascinating. This study was designed to determine the potential therapeutic effects of a newly developed novel urotensin II receptor antagonist, N-(1-(3-bromo-4-(piperidin-4-yloxy)benzyl)piperidin-4-yl)benzo[b]thiophene-3-carboxamide (KR-36996), in experimental models of heart failure...
February 3, 2017: European Journal of Pharmacology
https://www.readbyqxmd.com/read/28159807/resveratrol-improves-exercise-performance-and-skeletal-muscle-oxidative-capacity-in-heart-failure
#10
Miranda M Sung, Nikole J Byrne, Ian M Robertson, Ty T Kim, Victor Samokhvalov, Jody Levasseur, Carrie-Lynn M Soltys, David Fung, Neil Tyreman, Emmanuel Denou, Kelvin Jones, John M Seubert, Jonathan D Schertzer, Jason R B Dyck
We investigated whether treatment of mice with established pressure overload-induced heart failure (HF) with the naturally occurring polyphenol resveratrol could improve functional symptoms of clinical HF such as fatigue and exercise intolerance. C57Bl/6N mice were subjected to either sham or transverse aortic constriction surgery to induce HF. Three weeks post-surgery, a cohort of mice with established HF (% ejection fraction; %EF<45) was administered resveratrol (~450 mg/kg/d) or vehicle for 2 weeks. Although %EF was similar between both groups of HF mice, those mice treated with resveratrol had increased total physical activity levels and exercise capacity...
February 3, 2017: American Journal of Physiology. Heart and Circulatory Physiology
https://www.readbyqxmd.com/read/28152298/salubrinal-alleviates-pressure-overload-induced-cardiac-hypertrophy-by-inhibiting-endoplasmic-reticulum-stress-pathway
#11
Shilpa Rani, Pradeep Kumar Sreenivasaiah, Chunghee Cho, Do Han Kim
Pathological hypertrophy of the heart is closely associated with endoplasmic reticulum stress (ERS), leading to maladaptations such as myocardial fibrosis, induction of apoptosis, and cardiac dysfunctions. Salubrinal is a known selective inhibitor of protein phosphatase 1 (PP1) complex involving dephosphorylation of phospho-eukaryotic translation initiation factor 2 subunit (p-eIF2)-α, the key signaling process in the ERS pathway. In this study, the effects of salubrinal were examined on cardiac hypertrophy using the mouse model of transverse aortic constriction (TAC) and cell model of neonatal rat ventricular myocytes (NRVMs)...
January 2017: Molecules and Cells
https://www.readbyqxmd.com/read/28143738/manipulating-pml-sumoylation-via-silencing-ubc9-and-rnf4-regulates-cardiac-fibrosis
#12
Yu Liu, Dan Zhao, Fang Qiu, Ling-Ling Zhang, Shang-Kun Liu, Yuan-Yuan Li, Mei-Tong Liu, Di Wu, Jia-Xin Wang, Xiao-Qing Ding, Yan-Xin Liu, Chang-Jiang Dong, Xiao-Qi Shao, Bao-Feng Yang, Wen-Feng Chu
The promyelocytic leukemia protein (PML) is essential in the assembly of dynamic subnuclear structures called PML nuclear bodies (PML-NBs), which are involved in regulating diverse cellular functions. However, the possibility of PML being involved in cardiac disease has not been examined. In mice undergoing transverse aortic constriction (TAC) and arsenic trioxide (ATO) injection, transforming growth factor β1 (TGF-β1) was upregulated along with dynamic alteration of PML SUMOylation. In cultured neonatal mouse cardiac fibroblasts (NMCFs), ATO, angiotensin II (Ang II), and fetal bovine serum (FBS) significantly triggered PML SUMOylation and the assembly of PML-NBs...
March 1, 2017: Molecular Therapy: the Journal of the American Society of Gene Therapy
https://www.readbyqxmd.com/read/28130336/peroxisome-proliferator-activated-receptor-%C3%AE-expression-induces-alterations-in-cardiac-myofilaments-in-a-pressure-overload-model-of-hypertrophy
#13
Chehade N Karam, Chad M Warren, Marcus Henze, Natasha Hausler Banke, E Douglas Lewandowski, R John Solaro
Although alterations in fatty acid (FA) metabolism have been shown to have a negative impact on contractility of the hypertrophied heart, the targets of action remain elusive. In this study we compared the function of skinned fiber bundles from transgenic (Tg) mice, that over express a relatively low level of the peroxisome proliferator-activated receptor α (PPARα), and non-transgenic (NTg) littermates. The mice (NTg-T and Tg-T) were stressed by transverse aortic constriction (TAC) and compared to shams (NTg-S and Tg-S)...
January 27, 2017: American Journal of Physiology. Heart and Circulatory Physiology
https://www.readbyqxmd.com/read/28125666/mononuclear-phagocytes-are-dispensable-for-cardiac-remodeling-in-established-pressure-overload-heart-failure
#14
Bindiya Patel, Mohamed Ameen Ismahil, Tariq Hamid, Shyam S Bansal, Sumanth D Prabhu
BACKGROUND: Although cardiac and splenic mononuclear phagocytes (MPs), i.e., monocytes, macrophages and dendritic cells (DCs), are key contributors to cardiac remodeling after myocardial infarction, their role in pressure-overload remodeling is unclear. We tested the hypothesis that these immune cells are required for the progression of remodeling in pressure-overload heart failure (HF), and that MP depletion would ameliorate remodeling. METHODS AND RESULTS: C57BL/6 mice were subjected to transverse aortic constriction (TAC) or sham operation, and assessed for alterations in MPs...
2017: PloS One
https://www.readbyqxmd.com/read/28100897/x-indening-oral-liquid-improves-cardiac-function-of-rats-with-chronic-cardiac-failure-via-tgf-%C3%A3-1-smad3-and-p38-mapk-pathway
#15
Yunliang Wei, Changsheng Guo, Jingsheng Zhao, Jun Yang, Weiguo Yi, Hong Liu, Xinwei Lin, Zhengchen Zhang
OBJECTIVE: Xindening oral liquid (Xin) is a widely used traditional Chinese medicine for the treatment of chronic heart failure (CHF). However, the exact mechanisms related to its therapeutic effects against CHF remain unclear. In the present study, we investigate the effects of Xin on cardiac function in CHF rats and the possible mechanisms involved. METHODS: Transverse aortic constriction (TAC) was conducted to induce a CHF rat model in this study. Sixty male Wistar rats were randomly assigned to six groups 28 days after TAC: sham; CHF model; Xin at concentrations of 5 ml/kg, 10 mL/kg, and 20 mL/kg; and QiLi 0...
January 17, 2017: Anatolian Journal of Cardiology
https://www.readbyqxmd.com/read/28100873/microrna-10a-targets-t-box-5-to-inhibit-the-development-of-cardiac-hypertrophy
#16
Dan Wang, Guanqun Zhai, Yangfei Ji, Haiyun Jing
The mechanism of cardiac hypertrophy involving microRNAs (miRNAs) is attracting increasing attention. Our study aimed to investigate the role of miR-10a in cardiac hypertrophy development and the underlying regulatory mechanism.Transverse abdominal aortic constriction (TAAC) surgery was performed to establish a cardiac hypertrophy rat model, and angiotensin II (AngII) was used to induce cardiac hypertrophy in cultured neonatal rat cardiomyocytes. Expression of T-box 5 (TBX5) and miR-10a was altered by cell transfection of siRNA or miRNA mimic/inhibitor...
February 7, 2017: International Heart Journal
https://www.readbyqxmd.com/read/28091697/heat-shock-transcription-factor-1-protects-against-pressure-overload-induced-cardiac-fibrosis-via-smad3
#17
Ning Zhou, Yong Ye, Xingxu Wang, Ben Ma, Jian Wu, Lei Li, Lin Wang, Dao Wen Wang, Yunzeng Zou
Fibrotic cardiac muscle exhibits high stiffness and low compliance which are major risk factors of heart failure. Although heat shock transcription factor 1 (HSF1) was identified as an intrinsic cardioprotective factor, the role that HSF1 plays in cardiac fibrosis remains unclear. Our study aims to investigate the role of HSF1 in pressure overload-induced cardiac fibrosis and the underlying mechanism. HSF1 phosphorylation was significantly downregulated in transverse aortic constriction (TAC)-treated mouse hearts and mechanically stretched cardiac fibroblasts (cFBs)...
January 13, 2017: Journal of Molecular Medicine: Official Organ of the "Gesellschaft Deutscher Naturforscher und Ärzte"
https://www.readbyqxmd.com/read/28062415/cardiomyocyte-specific-ablation-of-cd36-accelerates-the-progression-from-compensated-cardiac-hypertrophy-to-heart-failure
#18
Miranda M Sung, Nikole J Byrne, Ty T Kim, Jody Levasseur, Grant Masson, Jamie J Boisvenue, Maria Febbraio, Jason R B Dyck
Previous studies have shown that loss of CD36 protects the heart from dysfunction induced by pressure overload in the presence of diet-induced insulin resistance and/or obesity. The beneficial effects of CD36 ablation in this context are mediated by preventing excessive cardiac fatty acid (FA) entry and reducing lipotoxic injury. However, whether or not the loss of CD36 can prevent pressure overload-induced cardiac dysfunction in the absence of chronic exposure to high circulating FAs is presently unknown. To address this, we utilized a tamoxifen-inducible cardiomyocyte-specific CD36 knockout (icCD36KO) mouse and genetically deleted CD36 in adulthood...
March 1, 2017: American Journal of Physiology. Heart and Circulatory Physiology
https://www.readbyqxmd.com/read/28045017/protective-effects-of-intercalated-disk-protein-afadin-on-chronic-pressure-overload-induced-myocardial-damage
#19
Dimitar P Zankov, Akio Shimizu, Miki Tanaka-Okamoto, Jun Miyoshi, Hisakazu Ogita
Adhesive intercellular connections at cardiomyocyte intercalated disks (IDs) support contractile force and maintain structural integrity of the heart muscle. Disturbances of the proteins at IDs deteriorate cardiac function and morphology. An adaptor protein afadin, one of the components of adherens junctions, is expressed ubiquitously including IDs. At present, the precise role of afadin in cardiac physiology or disease is unknown. To explore this, we generated conditional knockout (cKO) mice with cardiomyocyte-targeted deletion of afadin...
January 3, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28011586/activation-of-ppar%C3%AE-in-the-early-stage-of-heart-failure-maintained-myocardial-function-and-energetics-in-pressure-overload-heart-failure
#20
Satoshi Kaimoto, Atsushi Hoshino, Makoto Ariyoshi, Yoshifumi Okawa, Shuhei Tateishi, Kazunori Ono, Motoki Uchihashi, Kuniyoshi Fukai, Eri Iwai-Kanai, Satoaki Matoba
Failing heart loses its metabolic flexibility, relying increasingly on glucose as its preferential substrate and decreasing fatty acid oxidation (FAO). Peroxisome proliferator-activated receptor α (PPARα) is a key regulator of this substrate shift. However, its role during heart failure is complex and remains unclear. Recent studies reported that heart failure develops in the heart of MHC-PPARαmice in a manner similar to that of diabetic cardiomyopathy, whereas cardiac dysfunction is enhanced in PPARα knockout mice in response to chronic pressure overload...
December 23, 2016: American Journal of Physiology. Heart and Circulatory Physiology
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