نتایج جستجو برای: cardiac fibrosis

تعداد نتایج: 376764  

Journal: :Circulation 2013
Cameron J Holloway Ntobeko Ntusi Joseph Suttie Masliza Mahmod Emma Wainwright Genevieve Clutton Gemma Hancock Philip Beak Abdelouahid Tajar Stefan K Piechnik Jurgen E Schneider Brian Angus Kieran Clarke Lucy Dorrell Stefan Neubauer

BACKGROUND HIV infection continues to be endemic worldwide. Although treatments are successful, it remains controversial whether patients receiving optimal therapy have structural, functional, or biochemical cardiac abnormalities that may underlie their increased cardiac morbidity and mortality. The purpose of this study was to characterize myocardial abnormalities in a contemporary group of HI...

Journal: :The Journal of pharmacology and experimental therapeutics 2011
Yeling Wang Miaozong Wu Rabaa Al-Rousan Hua Liu Jacqueline Fannin Satyanarayana Paturi Ravi Kumar Arvapalli Anjaiah Katta Sunil K Kakarla Kevin M Rice William E Triest Eric R Blough

Excess cardiac iron levels are associated with cardiac damage and can result in increased morbidity and mortality. Here, we hypothesize that elevations in tissue iron can activate caspase-dependent signaling, which leads to increased cardiac apoptosis and fibrosis, and that these alterations can be attenuated by iron chelation. Using an iron-overloaded gerbil model, we show that increased cardi...

Journal: :American journal of physiology. Heart and circulatory physiology 2009
Qianli Yu Randy Vazquez Elham Vali Khojeini Chirag Patel Raj Venkataramani Douglas F Larson

Osteopontin (OPN), a key component of the extracellular matrix, is associated with the fibrotic process during tissue remodeling. OPN and the cytokine interleukin (IL)-18 have been shown to be overexpressed in an array of human cardiac pathologies. In the present study, we determined the role of IL-18 in the regulation of cardiac OPN expression and the subsequent interstitial fibrosis and diast...

Journal: :European heart journal 2012
Sebastian Szardien Holger M Nef Sandra Voss Christian Troidl Christoph Liebetrau Jedrzej Hoffmann Maximilian Rauch Katharina Mayer Kathrin Kimmich Andreas Rolf Johannes Rixe Kerstin Troidl Baktybek Kojonazarov Ralph T Schermuly Sawa Kostin Albrecht Elsässer Christian W Hamm Helge Möllmann

AIMS Aortic stenosis causes cardiac hypertrophy and fibrosis, which often persists despite pressure unloading after aortic valve replacement. The persistence of myocardial fibrosis in particular leads to impaired cardiac function and increased mortality. We investigated whether granulocyte colony-stimulating factor (G-CSF) beneficially influences cardiac remodelling after pressure unloading. ...

2012
Craig Bolte Yufang Zhang Allen York Tanya V. Kalin Jo El J. Schultz Jeffery D. Molkentin Vladimir V. Kalinichenko

Heart disease remains a leading cause of morbidity and mortality in the industrialized world. Hypertrophic cardiomyopathy is the most common genetic cardiovascular disorder and the most common cause of sudden cardiac death. Foxm1 transcription factor (also known as HFH-11B, Trident, Win or MPP2) plays an important role in the pathogenesis of various cancers and is a critical mediator of post-in...

2016
Bianca C. Bernardo Sally S. Nguyen Xiao-Ming Gao Yow Keat Tham Jenny Y. Y. Ooi Natalie L. Patterson Helen Kiriazis Yidan Su Colleen J. Thomas Ruby C. Y. Lin Xiao-Jun Du Julie R. McMullen

Expression of miR-154 is upregulated in the diseased heart and was previously shown to be upregulated in the lungs of patients with pulmonary fibrosis. However, the role of miR-154 in a model of sustained pressure overload-induced cardiac hypertrophy and fibrosis had not been assessed. To examine the role of miR-154 in the diseased heart, adult male mice were subjected to transverse aortic cons...

Journal: :Circulation 2009
Raffaella Lombardi Gabriela Rodriguez Suet Nee Chen Crystal M Ripplinger Wenwen Li Junjie Chen James T Willerson Sandro Betocchi Samuel A Wickline Igor R Efimov Ali J Marian

BACKGROUND Cardiac hypertrophy, the clinical hallmark of hypertrophic cardiomyopathy (HCM), is a major determinant of morbidity and mortality not only in HCM but also in a number of cardiovascular diseases. There is no effective therapy for HCM and generally for cardiac hypertrophy. Myocardial oxidative stress and thiol-sensitive signaling molecules are implicated in pathogenesis of hypertrophy...

Journal: :Circulation. Cardiovascular genetics 2015
Christoph D Rau Jessica Wang Rozeta Avetisyan Milagros C Romay Lisa Martin Shuxun Ren Yibin Wang Aldons J Lusis

BACKGROUND Chronic stress-induced cardiac pathology exhibits both a wide range in severity and a high degree of heterogeneity in clinical manifestation in human patients. This variability is contributed to by complex genetic and environmental etiologies within the human population. Genetic approaches to elucidate the genetics underlying the acquired forms of cardiomyopathies, including genome-w...

2017
Jin Zou Yanhua Liu Bingong Li Zeqi Zheng Xuan Ke Yanqin Hao Xuelian Li Xingxing Li Fuyou Liu Zhiyong Zhang

Endothelial-to-mesenchymal transition (EndMT) mainly exists in cardiovascular development and disease progression, and is well known to contribute to cardiac fibrosis. Recent studies indicated that autophagy also participates in the regulation of cardiac fibrosis. However, the precise role of autophagy in cardiac fibrosis and the underlying molecular mechanism remain unclear. The present study ...

Journal: :Physiological reports 2016
Beverly Giam Po-Yin Chu Sanjaya Kuruppu A Ian Smith Duncan Horlock Helen Kiriazis Xiao-Jun Du David M Kaye Niwanthi W Rajapakse

Oxidative stress plays a central role in the pathogenesis of heart failure. We aimed to determine whether the antioxidantN-acetylcysteine can attenuate cardiac fibrosis and remodeling in a mouse model of heart failure. Minipumps were implanted subcutaneously in wild-type mice (n = 20) and mice with cardiomyopathy secondary to cardiac specific overexpression of mammalian sterile 20-like kinase 1...

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