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https://www.readbyqxmd.com/read/29908129/the-role-of-microrna-181a-in-myocardial-fibrosis-following-myocardial-infarction-in-a-rat-model
#1
Peng Chen, Jialin Pan, Xinming Zhang, Zhewei Shi, Xiangjun Yang
BACKGROUND The role of miR-181a in the development of cardiac disease and in particular, myocardial fibrosis following myocardial infarction (MI) remains unknown. The aim of this study was to explore the role of miR-181a in myocardial fibrosis in a rat model of MI and the expression of TGF-β receptor III (TβRIII). MATERIAL AND METHODS Forty adult male Wistar rats were randomly divided into an MI model group (n=30) and a control group with (n=10). The rat MI model involved ligating the left anterior descending (LAD) coronary artery in the model group; the control group was treated with a sham operation...
June 16, 2018: Medical Science Monitor: International Medical Journal of Experimental and Clinical Research
https://www.readbyqxmd.com/read/29906461/sphingomyelin-phosphodiesterase-1-smpd1-mediates-the-attenuation-of-myocardial-infarction-induced-cardiac-fibrosis-by-astaxanthin
#2
Yu Shi, Peng Lin, Xiaoning Wang, Guangmei Zou, Kefeng Li
Uncontrolled cardiac fibrosis following myocardial infarction (MI) is a critical pathological change leading to heart failure. Current pharmacotherapies are limited by unsatisfactory efficacy and undesired systemic side effects. Astaxanthin (ASX) is a natural carotenoid with strong antioxidant and anti-inflammatory activities. The effects of ASX on MI-induced cardiac fibrosis and the underlying mechanisms remain largely unknown. In this study, after the establishment of MI model, mice were administrated with ASX (200 mg/kg⋅d) for 4 weeks...
June 12, 2018: Biochemical and Biophysical Research Communications
https://www.readbyqxmd.com/read/29906228/changes-in-cardiac-resident-fibroblast-physiology-and-phenotype-in-aging
#3
JoAnn Trial, Katarzyna A Cieslik
The cardiac fibroblast plays a central role in tissue homeostasis and in repair after injury. With aging, dysregulated cardiac fibroblasts have a reduced capacity to respond to transforming growth factor-β (TGF-β) and poorly differentiate into contractile myofibroblasts. That results in the formation of an insufficient scar after myocardial infarction (MI). By contrast, in the uninjured aged heart fibroblasts are activated and acquire a pro-fibrotic phenotype that leads to interstitial fibrosis, ventricular stiffness, and diastolic dysfunction, all conditions that may lead to heart failure...
June 15, 2018: American Journal of Physiology. Heart and Circulatory Physiology
https://www.readbyqxmd.com/read/29906222/analysis-of-the-microrna-signature-driving-adaptive-right-ventricular-hypertrophy-in-an-ovine-model-of-congenital-heart-disease
#4
Rebecca Johnson Kameny, Youping He, Terry Zhu, Wenhui Gong, Gary W Raff, Cheryl J Chapin, Sanjeev A Datar, Jason Boehme, Akiko Hata, Jeffrey R Fineman
The right ventricular (RV) response to pulmonary arterial hypertension (PAH) is heterogeneous. Most patients have maladaptive changes with RV dilation and failure while some-especially patients with PAH secondary to congenital heart disease (CHD)-have an adaptive response with hypertrophy and preserved systolic function. Mechanisms for RV adaptation to PAH are unknown despite RV function being a primary determinant of mortality. In our CHD ovine model with fetally-implanted aortopulmonary shunt (shunt lambs), we previously demonstrated an adaptive physiologic RV response to increased afterload with hypertrophy...
June 15, 2018: American Journal of Physiology. Heart and Circulatory Physiology
https://www.readbyqxmd.com/read/29905796/heart-failure-with-preserved-ejection-fraction-from-mechanisms-to-therapies
#5
Carolyn S P Lam, Adriaan A Voors, Rudolf A de Boer, Scott D Solomon, Dirk J van Veldhuisen
This review aims to provide a translational perspective on recent developments in heart failure with preserved ejection fraction (HFpEF), linking mechanistic insights to potential therapies. A key concept in this review is that HFpEF is a haemodynamic condition wherein the heart fails to keep up with the circulatory demands of the body, or does so at the expense of raised left ventricular filling pressures. We, therefore, propose that the 'final common pathway' for development of congestion, i.e. basic haemodynamic mechanisms of increased left ventricular end-diastolic pressure, left atrial hypertension, pulmonary venous congestion, and plasma volume expansion, represents important initial targets for therapy in HFpEF...
June 13, 2018: European Heart Journal
https://www.readbyqxmd.com/read/29904044/cardiorespiratory-adaptation-in-a-6-minute-walk-test-by-fibrotic-idiopathic-interstitial-pneumonia-patients-who-did-or-did-not-respond-to-pulmonary-rehabilitation
#6
Baptiste Chéhère, Valérie Bougault, Cécile Chenivesse, Jean-Marie Grosbois, Benoit Wallaert
BACKGROUND: Pulmonary rehabilitation (PR) improves performance in the 6-min walk test (6MWT) in a subset of patients with fibrotic idiopathic interstitial pneumonia (f-IIP); however, a large proportion of patients do not respond to PR. AIM: To investigate the effects of a PR program on cardiorespiratory responses during a 6MWT and to identify the characteristics of patients who do not show improved performance after PR. DESIGN: An observational study...
June 14, 2018: European Journal of Physical and Rehabilitation Medicine
https://www.readbyqxmd.com/read/29895976/an-essential-role-for-wnt-%C3%AE-catenin-signaling-in-mediating-hypertensive-heart-disease
#7
Yue Zhao, Chunhong Wang, Cong Wang, Xue Hong, Jinhua Miao, Yulin Liao, Lili Zhou, Youhua Liu
Activation of the renin-angiotensin system (RAS) is associated with hypertension and heart disease. However, how RAS activation causes cardiac lesions remains elusive. Here we report the involvement of Wnt/β-catenin signaling in this process. In rats with chronic infusion of angiotensin II (Ang II), eight Wnt ligands were induced and β-catenin activated in both cardiomyocytes and cardiac fibroblasts. Blockade of Wnt/β-catenin signaling by small molecule inhibitor ICG-001 restrained Ang II-induced cardiac hypertrophy by normalizing heart size and inhibiting hypertrophic marker genes...
June 12, 2018: Scientific Reports
https://www.readbyqxmd.com/read/29893180/potential-adverse-cardiac-remodelling-in-highly-trained-athletes-still-unknown-clinical-significance
#8
Luigi Gabrielli, Marta Sitges, Mario Chiong, Jorge Jalil, María Ocaranza, Silvana Llevaneras, Sebastian Herrera, Rodrigo Fernandez, Rodrigo Saavedra, Fernando Yañez, Luis Vergara, Alexis Diaz, Sergio Lavandero, Pablo Castro
Moderate endurance exercise has long been considered an essential element to maintain cardiovascular health, and sedentary behaviour in the general population has been related to a significant increase in all-causes of mortality, cardiovascular disease mortality and cardiovascular disease incidence. However, a growing group of people performs an intense exercise that leads to multiple heart adaptive changes that are collectively called "athlete's heart". In this review, we discussed the evidence of cardiac remodelling process secondary to repetitive and strenuous exercise in some predisposed athletes that produces intense and probably deleterious changes in cardiac morphology and function with no clear clinical significance in long-term follow-up...
June 12, 2018: European Journal of Sport Science
https://www.readbyqxmd.com/read/29892471/heart-failure-in-sub-saharan-africa
#9
REVIEW
Joseph Gallagher, Kenneth McDonald, Mark Ledwidge, Chris J Watson
Heart failure is a growing problem in sub-Saharan Africa. This arises as the prevalence of risk factors for cardiovascular disease rises, life expectancy increases and causes of heart failure more common in Africa, such as rheumatic heart disease and endomyocardial fibrosis, continue to be a significant issue. Lack of access to diagnostics is an issue with the expense and technical expertise required for echocardiography limiting access. Biomarker strategies may play a role here. Access to essential medicines is also limited and requires a renewed focus by the international community to ensure that appropriate medications are readily available, similar to that which has been implemented for HIV and malaria...
May 2018: Cardiac Failure Review
https://www.readbyqxmd.com/read/29892269/paracrine-effects-of-fgf23-on-the-heart
#10
REVIEW
Maren Leifheit-Nestler, Dieter Haffner
Fibroblast growth factor (FGF) 23 is a phosphaturic hormone primarily secreted by osteocytes to maintain phosphate and mineral homeostasis. In patients with and without chronic kidney disease, enhanced circulating FGF23 levels associate with pathologic cardiac remodeling, i.e., left ventricular hypertrophy (LVH) and myocardial fibrosis and increased cardiovascular mortality. Experimental studies demonstrate that FGF23 promotes hypertrophic growth of cardiac myocytes via FGF receptor 4-dependent activation of phospholipase Cγ/calcineurin/nuclear factor of activated T cell signaling independent of its co-receptor klotho...
2018: Frontiers in Endocrinology
https://www.readbyqxmd.com/read/29892230/loss-of-akap1-exacerbates-pressure-overload-induced-cardiac-hypertrophy-and-heart-failure
#11
Gabriele G Schiattarella, Nicola Boccella, Roberta Paolillo, Fabio Cattaneo, Valentina Trimarco, Anna Franzone, Stefania D'Apice, Giuseppe Giugliano, Laura Rinaldi, Domenica Borzacchiello, Alessandra Gentile, Assunta Lombardi, Antonio Feliciello, Giovanni Esposito, Cinzia Perrino
Left ventricular hypertrophy (LVH) is a major contributor to the development of heart failure (HF). Alterations in cyclic adenosine monophosphate (cAMP)-dependent signaling pathways participate in cardiomyocyte hypertrophy and mitochondrial dysfunction occurring in LVH and HF. cAMP signals are received and integrated by a family of cAMP-dependent protein kinase A (PKA) anchor proteins (AKAPs), tethering PKA to discrete cellular locations. AKAPs encoded by the Akap1 gene (mitoAKAPs) promote PKA mitochondrial targeting, regulating mitochondrial structure and function, reactive oxygen species production, and cell survival...
2018: Frontiers in Physiology
https://www.readbyqxmd.com/read/29892004/perfect-chronic-skeletal-muscle-regeneration-in-adult-spiny-mice-acomys-cahirinus
#12
Malcolm Maden, Jason Orr Brant, Andres Rubiano, Aaron Gabriel W Sandoval, Chelsey Simmons, Robert Mitchell, Henry Collin-Hooper, Jason Jacobson, Saleh Omairi, Ketan Patel
The spiny mouse, Acomys cahirinus, is an adult mammal capable of remarkable feats of scar-free tissue regeneration after damage to several organs including the skin and the heart. Here we investigate the regenerative properties of the skeletal muscle of A. cahirinus tibialis anterior in comparison to the lab mouse, Mus musculus. The A. cahirinus TA showed a similar distribution of myosin heavy chain fibre types and a reduced proportion of oxidative fibres compared to M. musculus. There were differences in the matrix components of the TA with regard to collagen VI and the biomechanical properties...
June 11, 2018: Scientific Reports
https://www.readbyqxmd.com/read/29890086/azithromycin-for-early-pseudomonas-infection-in-cystic-fibrosis-the-optimize-randomized-trial
#13
Nicole Mayer-Hamblett, George Retsch-Bogart, Margaret Kloster, Frank Accurso, Margaret Rosenfeld, Gary Albers, Philip Black, Perry Brown, AnneMarie Cairns, Stephanie D Davis, Gavin R Graff, Gwendolyn S Kerby, David Orenstein, Rachael Buckingham, Bonnie W Ramsey
RATIONALE: New isolation of Pseudomonas aeruginosa (Pa) is generally treated with inhaled antipseudomonal antibiotics such as tobramycin inhalation solution (TIS). A therapeutic approach complementing traditional antimicrobial therapy by reducing the risk of pulmonary exacerbation (PEx) and inflammation may ultimately prolong time to Pa recurrence. OBJECTIVES: To test the hypothesis that the addition of azithromycin to TIS in children with CF and early Pa decreases the risk of PEx and prolongs time to Pa recurrence...
June 11, 2018: American Journal of Respiratory and Critical Care Medicine
https://www.readbyqxmd.com/read/29889834/pathological-presentation-of-cardiac-mitochondria-in-a-rat-model-for-chronic-kidney-disease
#14
Einat Bigelman, Lena Cohen, Genya Aharon-Hananel, Ran Levy, Zach Rozenbaum, Ann Saada, Gad Keren, Michal Entin-Meer
BACKGROUND: Mitochondria hold crucial importance in organs with high energy demand especially the heart. We investigated whether chronic kidney disease (CKD), which eventually culminates in cardiorenal syndrome, could affect cardiac mitochondria and assessed the potential involvement of angiotensin II (AngII) in the process. METHODS: Male Lewis rats underwent 5/6 nephrectomy allowing CKD development for eight months or for eleven weeks. Short-term CKD rats were administered with AngII receptor blocker (ARB)...
2018: PloS One
https://www.readbyqxmd.com/read/29889825/long-noncoding-rna-lncrna-n379519-promotes-cardiac-fibrosis-in-post-infarct-myocardium-by-targeting-mir-30
#15
Xiaxia Wang, Chunming Yong, Kai Yu, Renchao Yu, Rui Zhang, Lingfan Yu, Shan Li, Shanglang Cai
BACKGROUND Abnormally expressed long noncoding RNAs (lncRNAs) are recognized as one of the key causes of cardiac diseases. However, the role of lncRNA in cardiac fibrosis remains largely unknown. MATERIAL AND METHODS The experiment was divided into 4 groups: a sham operation group, a myocardial infarction (MI) group, a lentivirus group (LV-si-n379519), and a lentivirus control (LV-NC) group. The adenovirus expression vectors LV-si-n379519 and LV-NC were constructed and transfected into mice. Echocardiography, HE staining, and Masson staining were performed to detect the heart function and collagen volume fraction in each group...
June 11, 2018: Medical Science Monitor: International Medical Journal of Experimental and Clinical Research
https://www.readbyqxmd.com/read/29887522/relaxin-family-member-insulin-like-peptide-6-ameliorates-cardiac-fibrosis-and-prevents-cardiac-remodeling-in-murine-heart-failure-models
#16
Sonomi Maruyama, Chia-Ling Wu, Sumiko Yoshida, Dongying Zhang, Pei-Hsuan Li, Fangzhou Wu, Jennifer Parker Duffen, Rouan Yao, Blake Jardin, Ibrahim M Adham, Ronald Law, Joel Berger, Richard Di Marchi, Kenneth Walsh
BACKGROUND: The insulin/insulin-like growth factor/relaxin family represents a group of structurally related but functionally diverse proteins. The family member relaxin-2 has been evaluated in clinical trials for its efficacy in the treatment of acute heart failure. In this study, we assessed the role of insulin-like peptide 6 (INSL6), another member of this protein family, in murine heart failure models using genetic loss-of-function and protein delivery methods. METHODS AND RESULTS: Insl6-deficient and wild-type (C57BL/6N) mice were administered angiotensin II or isoproterenol via continuous infusion with an osmotic pump or via intraperitoneal injection once a day, respectively, for 2 weeks...
June 10, 2018: Journal of the American Heart Association
https://www.readbyqxmd.com/read/29884823/microrna-410-5p-exacerbates-high-fat-diet-induced-cardiac-remodeling-in-mice-in-an-endocrine-fashion
#17
Tong Zou, Mei Zhu, Yi-Cheng Ma, Fei Xiao, Xue Yu, Li Xu, Lan-Qing Ma, Jiefu Yang, Jian-Zeng Dong
Metabolic disorders, such as obesity and type 2 diabetes, are associated with an increased risk of cardiomyopathy. To date, microRNA (miRNAs) functions in cardiac remodeling induced by obesity remain to be elucidated. We found that rats fed a high fat diet (HFD) manifested cardiac fibrosis and LV dysfunction. In the heart of rats fed HFD, the phosphorylation levels of Smad 2 and the expression of fibrotic genes, such as connective tissue growth factor, collagen-1α1 (Col1α1), Col3α1, and Col4α1, were up-regulated, which accompanied by an increase in Smad 7 protein levels, but not its mRNA levels...
June 8, 2018: Scientific Reports
https://www.readbyqxmd.com/read/29884599/predictors-of-future-onset-of-atrial-fibrillation-in-hypertrophic-cardiomyopathy
#18
Hubert Cochet, Lucas Morlon, Marie-Philippe Vergé, Marjorie Salel, Claudia Camaioni, Amélie Reynaud, Jérôme Peyrou, Philippe Ritter, Pierre Jais, François Laurent, Stéphane Lafitte, Michel Montaudon, Patricia Réant
BACKGROUND: Novel predictors of atrial fibrillation (AF) in hypertrophic cardiomyopathy (HCM) are desirable. AIM: To detect new multimodality imaging variables predictive of de novo AF in HCM. METHODS: Consecutive patients with HCM underwent clinical assessment and 48-hour Holter electrocardiography to detect AF episodes. Left ventricular (LV) morphology, function and fibrosis, and the left atrium (LA) were characterized by cardiac magnetic resonance...
June 5, 2018: Archives of Cardiovascular Diseases
https://www.readbyqxmd.com/read/29878127/a-novel-method-for-high-precision-aortic-constriction-that-allows-for-generation-of-specific-cardiac-phenotypes-in-mice
#19
Arne O Melleby, Andreas Romaine, Jan Magnus Aronsen, Ioanni Veras, Lili Zhang, Ivar Sjaastad, Ida G Lunde, Geir Christensen
Aims: Generation of reproducible cardiac disease phenotypes in mice is instrumental for investigating mechanisms leading to heart failure. For decades, suture-based thoracic aortic constriction has been the preferred method for increasing left ventricular (LV) afterload in rodents, but the degree of stenosis resulting from this method is variable. In an effort to improve this methodology, we subjected mice to constriction of the ascending aorta using o-rings with fixed inner diameters (IDs)...
June 5, 2018: Cardiovascular Research
https://www.readbyqxmd.com/read/29871865/a-novel-rabbit-model-of-duchenne-muscular-dystrophy-generated-by-crispr-cas9
#20
Tingting Sui, Yeh Siang Lau, Di Liu, Tingjun Liu, Li Xu, Yandi Gao, Liangxue Lai, Zhanjun Li, Renzhi Han
Duchenne muscular dystrophy (DMD) is an X-linked muscle-wasting disorder caused by mutations in the dystrophin gene, with an incidence of 1 in 3500 in new male births. Mdx mice are widely used as an animal model for DMD. However, these mice do not faithfully recapitulate DMD patients in many aspects, rendering the preclinical findings in this model questionable. Although larger animal models of DMD, such as dogs and pigs, have been generated, usage of these animals is expensive and only limited to several facilities in the world...
June 4, 2018: Disease Models & Mechanisms
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