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https://www.readbyqxmd.com/read/28330809/piperine-attenuates-pathological-cardiac-fibrosis-via-ppar-%C3%AE-akt-pathways
#1
Zhen-Guo Ma, Yu-Pei Yuan, Xin Zhang, Si-Chi Xu, Sha-Sha Wang, Qi-Zhu Tang
Mitogen-activated protein kinases (MAPKs) and AMP-activated protein kinase α (AMPKα) play critical roles in the process of cardiac hypertrophy. Previous studies have demonstrated that piperine activates AMPKα and reduces the phosphorylation of extracellular signal-regulated kinase (ERK). However, the effect of piperine on cardiac hypertrophy remains completely unknown. Here, we show that piperine-treated mice had similar hypertrophic responses as mice treated with vehicle but exhibited significantly attenuated cardiac fibrosis after pressure overload or isoprenaline (ISO) injection...
March 14, 2017: EBioMedicine
https://www.readbyqxmd.com/read/28327570/puf60-variants-cause-a-syndrome-of-id-short-stature-microcephaly-coloboma-craniofacial-cardiac-renal-and-spinal-features
#2
Karen J Low, Morad Ansari, Rami Abou Jamra, Angus Clarke, Salima El Chehadeh, David R FitzPatrick, Mark Greenslade, Alex Henderson, Jane Hurst, Kory Keller, Paul Kuentz, Trine Prescott, Franziska Roessler, Kaja K Selmer, Michael C Schneider, Fiona Stewart, Katrina Tatton-Brown, Julien Thevenon, Magnus D Vigeland, Julie Vogt, Marjolaine Willems, Jonathan Zonana, D D D Study, Sarah F Smithson
PUF60 encodes a nucleic acid-binding protein, a component of multimeric complexes regulating RNA splicing and transcription. In 2013, patients with microdeletions of chromosome 8q24.3 including PUF60 were found to have developmental delay, microcephaly, craniofacial, renal and cardiac defects. Very similar phenotypes have been described in six patients with variants in PUF60, suggesting that it underlies the syndrome. We report 12 additional patients with PUF60 variants who were ascertained using exome sequencing: six through the Deciphering Developmental Disorders Study and six through similar projects...
March 22, 2017: European Journal of Human Genetics: EJHG
https://www.readbyqxmd.com/read/28322201/association-of-cardiac-galectin-3-expression-myocarditis-and-fibrosis-in-chronic-chagas-disease-cardiomyopathy
#3
Bruno Solano de Freitas Souza, Daniela Nascimento Silva, Rejane Hughes Carvalho, Gabriela Louise de Almeida Sampaio, Bruno Diaz Paredes, Luciana Aragão França, Carine Machado Azevedo, Juliana Fraga Vasconcelos, Cassio Santana Meira, Paulo Chenaud Neto, Simone Garcia Macambira, Kátia Nunes da Silva, Kyan James Allahdadi, Fabio Tavora, João David de Souza Neto, Ricardo Ribeiro Dos Santos, Milena Botelho Pereira Soares
Chronic Chagas disease cardiomyopathy, caused by Trypanosoma cruzi infection, is a major cause of heart failure in Latin America. Galectin-3 (Gal-3) has been linked to cardiac remodeling and poor prognosis in heart failure of different etiologies. Herein, we investigated the involvement of Gal-3 in the disease pathogenesis and its role as a target for disease intervention. Gal-3 expression in mouse hearts was evaluated during T. cruzi infection by confocal microscopy and flow cytometry analysis, showing a high expression in macrophages, T cells, and fibroblasts...
March 16, 2017: American Journal of Pathology
https://www.readbyqxmd.com/read/28321644/vinpocetine-attenuates-pathological-cardiac-remodeling-by-inhibiting-cardiac-hypertrophy-and-fibrosis
#4
Mei-Ping Wu, Yi-Shuai Zhang, Xiangbin Xu, Qian Zhou, Jian-Dong Li, Chen Yan
PURPOSE: Pathological cardiac remodeling, characterized by cardiac hypertrophy and fibrosis, is a pathological feature of many cardiac disorders that leads to heart failure and cardiac arrest. Vinpocetine, a derivative of the alkaloid vincamine, has been used for enhancing cerebral blood flow to treat cognitive impairment. However, its role in pathological cardiac remodeling remains unknown. The aim of this study is to examine the effect of vinpocetine on pathological cardiac remodeling induced by chronic stimulation with angiotensin II (Ang II)...
March 20, 2017: Cardiovascular Drugs and Therapy
https://www.readbyqxmd.com/read/28321399/renocardiovascular-biomarkers-from-the-perspective-of-managing-chronic-kidney-disease-and-cardiovascular-disease
#5
REVIEW
Shinichiro Niizuma, Yoshitaka Iwanaga, Takaharu Yahata, Shunichi Miyazaki
Mortality among the patients with chronic kidney disease (CKD) and end-stage renal disease (ESRD) remains high because of the very high incidence of cardiovascular disease (CVD) such as coronary artery disease, cardiac hypertrophy, and heart failure. Identifying CVD in patients with CKD/ESRD remains a significant hurdle and the early diagnosis and therapy for CVD is crucial in these patients. Therefore, it is necessary for the better management to identify and utilize cardiovascular (CV) biomarkers in profiling CVD risk and enabling stratification of early mortality...
2017: Frontiers in Cardiovascular Medicine
https://www.readbyqxmd.com/read/28320863/rac1-gtpase-regulates-11%C3%AE-hydroxysteroid-dehydrogenase-type-2-and-fibrotic-remodeling
#6
Daniel Lavall, Pia Schuster, Nadine Jacobs, Andrey Kazakov, Michael Böhm, Ulrich Laufs
The aim of the study was to characterize the role of Rac1 GTPase for the mineralocorticoid receptor (MR) mediated pro-fibrotic remodeling. Transgenic mice with cardiac overexpression of constitutively active Rac1 (RacET) develop an age-dependent phenotype with atrial dilatation, fibrosis and atrial fibrillation. Expression of MR was similar in RacET and wild-type (WT) mice. The expression of 11β hydroxysteroid dehydrogenase type 2 (11β-HSD2) was age-dependently upregulated in the atria and the left ventricles of RacET mice on mRNA and protein level...
March 20, 2017: Journal of Biological Chemistry
https://www.readbyqxmd.com/read/28316086/cardiac-fibrosis-in-the-ageing-heart-contributors-and-mechanisms
#7
Lu Lu, Jingbin Guo, Yue Hua, Kevin Huang, Ruth Magaye, Jake Cornell, Darren J Kelly, Christopher Reid, Danny Liew, Yingchun Zhou, Aihua Chen, Wei Xiao, Qiang Fu, Bing Hui Wang
Cardiac fibrosis refers to an excessive deposition of extracellular matrix (ECM) in cardiac tissue. Fibrotic tissue is stiffer and less compliant, resulting in subsequent cardiac dysfunction and heart failure. Cardiac fibrosis in the ageing heart may involve activation of fibrogenic signalling and inhibition of anti-fibrotic signalling, leading to an imbalance of ECM turnover. Excessive accumulation of ECM such as collagen in older patients contributes to progressive ventricular dysfunction. Overexpression of collagen is derived from various sources, including higher levels of fibrogenic growth factors, proliferation of fibroblasts and cellular trans-differentiation...
March 18, 2017: Clinical and Experimental Pharmacology & Physiology
https://www.readbyqxmd.com/read/28315522/human-cardiac-fibroblasts-adaptive-responses-to-controlled-combined-mechanical-strain-and-oxygen-changes-in-vitro
#8
Giovanni Stefano Ugolini, Andrea Pavesi, Marco Rasponi, Gianfranco Beniamino Fiore, Roger Kamm, Monica Soncini
Upon cardiac pathological conditions such as ischemia, microenvironmental changes instruct a series of cellular responses that trigger cardiac fibroblasts-mediated tissue adaptation and inflammation. A comprehensive model of how early environmental changes may induce cardiac fibroblasts (CF) pathological responses is far from being elucidated, partly due to the lack of approaches involving complex and simultaneous environmental stimulation. Here, we provide a first analysis of human primary CF behavior by means of a multi-stimulus microdevice for combined application of cyclic mechanical strain and controlled oxygen tension...
March 18, 2017: ELife
https://www.readbyqxmd.com/read/28303407/evodiamine-attenuates-tgf-%C3%AE-1-induced-fibroblast-activation-and-endothelial-to-mesenchymal-transition
#9
Qing-Qing Wu, Yang Xiao, Xiao-Han Jiang, Yuan Yuan, Zheng Yang, Wei Chang, Zhou-Yan Bian, Qi-Zhu Tang
The aim of this study is to investigate the effect of evodiamine on fibroblast activation in cardiac fibroblasts and endothelial to mesenchymal transition (EndMT) in human umbilical vein endothelial cells (HUVECs). Neonatal rat cardiac fibroblasts were stimulated with transforming growth factor beta 1 (TGF-β1) to induce fibroblast activation. After co-cultured with evodiamine (5, 10 μM), the proliferation and pro-fibrotic proteins expression of cardiac fibroblasts were evaluated. HUVECs were also stimulated with TGF-β1 to induce EndMT and treated with evodiamine (5, 10 μM) at the same time...
March 16, 2017: Molecular and Cellular Biochemistry
https://www.readbyqxmd.com/read/28303153/de-novo-human-cardiac-myocytes-for-medical-research-promises-and-challenges
#10
REVIEW
Veronique Hamel, Kang Cheng, Shudan Liao, Aizhu Lu, Yong Zheng, Yawen Chen, Yucai Xie, Wenbin Liang
The advent of cellular reprogramming technology has revolutionized biomedical research. De novo human cardiac myocytes can now be obtained from direct reprogramming of somatic cells (such as fibroblasts), from induced pluripotent stem cells (iPSCs, which are reprogrammed from somatic cells), and from human embryonic stem cells (hESCs). Such de novo human cardiac myocytes hold great promise for in vitro disease modeling and drug screening and in vivo cell therapy of heart disease. Here, we review the technique advancements for generating de novo human cardiac myocytes...
2017: Stem Cells International
https://www.readbyqxmd.com/read/28300638/astaxanthin-attenuated-pressure-overload-induced-cardiac-dysfunction-and-myocardial-fibrosis-partially-by-activating-sirt1
#11
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/28296029/cd38-promotes-angiotensin-ii-induced-cardiac-hypertrophy
#12
Xiao-Hui Guan, Xuan Hong, Ning Zhao, Xiao-Hong Liu, Yun-Fei Xiao, Ting-Tao Chen, Li-Bin Deng, Xiao-Lei Wang, Jian-Bin Wang, Guang-Ju Ji, Mingui Fu, Ke-Yu Deng, Hong-Bo Xin
Cardiac hypertrophy is an early hallmark during the clinical course of heart failure and regulated by various signalling pathways. Recently, we observed that mouse embryonic fibroblasts from CD38 knockout mice were significantly resistant to oxidative stress such as H2 O2 -induced injury and hypoxia/reoxygenation-induced injury. In addition, we also found that CD38 knockout mice protected heart from ischaemia reperfusion injury through activating SIRT1/FOXOs-mediated antioxidative stress pathway. However, the role of CD38 in cardiac hypertrophy is not explored...
March 12, 2017: Journal of Cellular and Molecular Medicine
https://www.readbyqxmd.com/read/28294304/il-21-promotes-myocardial-ischemia-reperfusion-injury-through-the-modulation-of-neutrophil-infiltration
#13
Kejing Wang, Shuang Wen, Jiao Jiao, Tingting Tang, Xin Zhao, Min Zhang, Bingjie Lv, Yuzhi Lu, Xingdi Zhou, Jingyong Li, Shaofang Nie, Yuhua Liao, Qing Wang, Xin Tu, Ziad Mallat, Ni Xia, Xiang Cheng
BACKGROUND AND PURPOSE: The immune system plays important roles in driving the acute inflammatory response following myocardial ischemia/reperfusion injury (MIRI). Interleukin-21 (IL-21) is a pleiotropic cytokine with multiple immunomodulatory effects and its role in MIRI remains unknown. EXPERIMENTAL APPROACH: Myocardial injury, neutrophil infiltration and expressions of neutrophil chemokines keratinocyte-derived chemokine (KC) and macrophage inflammatory protein-2 (MIP-2) were studied in a mouse model of MIRI...
March 14, 2017: British Journal of Pharmacology
https://www.readbyqxmd.com/read/28289072/downregulation-of-mir-15a-b-accelerates-fibrotic-remodelling-in-the-type-2-diabetic-human-and-mouse-heart
#14
Shruti Rawal, Pujika Emani Munasinghe, Prashanth Thevakar, Jason Kar Sheng Lew, Gregory T Jones, Michael Ja Willams, Philip Davis, Richard W Bunton, Ivor F Galvin, Patrick Manning, Regis R Lamberts, Rajesh G Katare
AIM: Myocardial fibrosis is a well established cause of increased myocardial stiffness and subsequent diastolic dysfunction in the diabetic heart. The molecular regulators that drive the process of fibrotic events in the diabetic heart are still unknown. We determined the role of the microRNA (miR)-15 family in fibrotic remodelling of the diabetic heart. METHODS AND RESULTS: Right atrial appendage (RAA) and left ventricular (LV) biopsy tissues collected from diabetic and non-diabetic patients undergoing coronary artery bypass graft surgery showed significant downregulation of miR-15a and -15b...
March 13, 2017: Clinical Science (1979-)
https://www.readbyqxmd.com/read/28281243/mimicking-cardiac-fibrosis-in-a-dish-fibroblast-density-rather-than-collagen-density-weakens-cardiomyocyte-function
#15
Ariane C C van Spreeuwel, Noortje A M Bax, Bastiaan J van Nierop, Annemieke Aartsma-Rus, Marie-José T H Goumans, Carlijn V C Bouten
Cardiac fibrosis is one of the most devastating effects of cardiac disease. Current in vitro models of cardiac fibrosis do not sufficiently mimic the complex in vivo environment of the cardiomyocyte. We determined the local composition and mechanical properties of the myocardium in established mouse models of genetic and acquired fibrosis and tested the effect of myocardial composition on cardiomyocyte contractility in vitro by systematically manipulating the number of fibroblasts and collagen concentration in a platform of engineered cardiac microtissues...
March 9, 2017: Journal of Cardiovascular Translational Research
https://www.readbyqxmd.com/read/28275645/novel-direct-reprogramming-technique-for-the-generation-of-culture-expandable-cardiac-progenitor-cells-from-fibroblasts
#16
EDITORIAL
Masaaki Ii
No abstract text is available yet for this article.
2017: Stem Cell Investigation
https://www.readbyqxmd.com/read/28272448/aggravated-myocardial-infarction-induced-cardiac-remodeling-and-heart-failure-in-histamine-deficient-mice
#17
Jinmiao Chen, Tao Hong, Suling Ding, Long Deng, Mieradilijiang Abudupataer, Weiwei Zhang, Minghong Tong, Jianguo Jia, Hui Gong, Yunzeng Zou, Timothy C Wang, Junbo Ge, Xiangdong Yang
Histamine has pleiotropic pathophysiological effects, but its role in myocardial infarction (MI)-induced cardiac remodeling remains unclear. Histidine decarboxylase (HDC) is the main enzyme involved in histamine production. Here, we clarified the roles of HDC-expressing cells and histamine in heart failure post-MI using HDC-EGFP transgenic mice and HDC-knockout (HDC(-/-)) mice. HDC(+)CD11b(+) myeloid cell numbers markedly increased in the injured hearts, and histamine levels were up-regulated in the circulation post-MI...
March 8, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28270772/lack-of-abcg2-leads-to-biventricular-dysfunction-and-remodeling-in-response-to-hypoxia
#18
Bence M Nagy, Chandran Nagaraj, Bakytbek Egemnazarov, Grazyna Kwapiszewska, Rudolf E Stauber, Alexander Avian, Horst Olschewski, Andrea Olschewski
Aims: The ATP-binding cassette (ABC)G2 transporter protects the heart from pressure overload-induced ventricular dysfunction but also protects cancer cells from chemotherapeutic agents. It is upregulated in the myocardium of heart failure patients and clears hypoxia-induced intracellular metabolites. This study employs ABCG2 knockout (KO) mice to elucidate the relevance of ABCG2 for cardiac and pulmonary vascular structure and function in chronic hypoxia, and uses human primary cardiac fibroblasts to investigate the potential role of ABCG2 in cardiac fibrosis...
2017: Frontiers in Physiology
https://www.readbyqxmd.com/read/28268305/modulation-of-cardiac-pacemaker-inter-beat-intervals-by-sinoatrial-fibroblasts-a-numerical-study
#19
Ariel Greisas, Sharon Zlochiver
The potential effect of sinoatrial fibroblasts on beat rate and variability of the cardiac pacemakers is not yet fully understood. Heterocellular coupling formation and fibroblast proliferation during diseased conditions may further signify the impact of those cells on sinoatrial node function. In this study we numerically modeled the impact of varying numbers of fibroblasts that are electrically coupled to a single pacemaker cell on several electrophysiological parameters. We employed cellular kinetics of the rabbit sinoatrial myocyte, and employed a range of potential gap junctional coupling between fibroblasts and myocytes...
August 2016: Conference Proceedings: Annual International Conference of the IEEE Engineering in Medicine and Biology Society
https://www.readbyqxmd.com/read/28266583/zyz-168-alleviates-cardiac-fibrosis-after-myocardial-infarction-through-inhibition-of-erk1-2-dependent-rock1-activation
#20
Shanshan Luo, Tran Ba Hieu, Fenfen Ma, Ying Yu, Zhonglian Cao, Minjun Wang, Weijun Wu, Yicheng Mao, Peter Rose, Betty Yuen-Kwan Law, Yi Zhun Zhu
Selective treatments for myocardial infarction (MI) induced cardiac fibrosis are lacking. In this study, we focus on the therapeutic potential of a synthetic cardio-protective agent named ZYZ-168 towards MI-induced cardiac fibrosis and try to reveal the underlying mechanism. ZYZ-168 was administered to rats with coronary artery ligation over a period of six weeks. Ecocardiography and Masson staining showed that ZYZ-168 substantially improved cardiac function and reduced interstitial fibrosis. The expression of α-smooth muscle actin (α-SMA) and Collagen I were reduced as was the activity of matrix metalloproteinase 9 (MMP-9)...
March 7, 2017: Scientific Reports
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