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Titlebook: Cardiac Fibrosis and Heart Failure: Cause or Effect?; Ian M.C. Dixon,Jeffrey T. Wigle Book 2015 Springer International Publishing Switzerl

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发表于 2025-3-21 19:00:45 | 显示全部楼层 |阅读模式
书目名称Cardiac Fibrosis and Heart Failure: Cause or Effect?
编辑Ian M.C. Dixon,Jeffrey T. Wigle
视频video
概述Focuses on autophagy and endoplasmic reticular stress as mechanisms to regulate cardiac fibrosis.Highlights the role of alterations in the extracellular matrix during the development of heart failure.
丛书名称Advances in Biochemistry in Health and Disease
图书封面Titlebook: Cardiac Fibrosis and Heart Failure: Cause or Effect?;  Ian M.C. Dixon,Jeffrey T. Wigle Book 2015 Springer International Publishing Switzerl
描述.The unique biology of cardiac fibroblasts and related cells, such as cardiac myofibroblasts and valvular interstitial cells, distinguish them from other fibroblastic cells, a concept that is only beginning to be widely appreciated. Further, the natural signals that stimulate and inhibit cardiac fibrosis within these cells are not well understood. This volume compiles articles that address the molecular mechanisms that control the synthesis and secretion of the cardiac ECM. The book showcases chapters that highlight discussion of role of Transforming Growth Factor β (TGFβ), an important fibrogenic cytokine and its downstream effectors SMAD in many cardiac diseases. Further, the contributions highlight information to discuss endogenous inhibitors of cardiac fibrosis, as well as advances in tissue engineering specific to matrix in the heart. Finally, discussions of unifying mechanisms of matrix remodeling in valves and myocardium are presented..The mechanisms involved in the stimulation of cardiac fibrosis are not fully understood. In most cases the marginal attenuation of cardiac fibrosis as a result of a given therapy is a beneficial side-effect linked to other primary effects on o
出版日期Book 2015
关键词Cardiac Fibrosis; Myofibroblasts; cardiac extracellular matrix; cardiac fibroblasts; microRNAs
版次1
doihttps://doi.org/10.1007/978-3-319-17437-2
isbn_softcover978-3-319-37995-1
isbn_ebook978-3-319-17437-2Series ISSN 2512-2142 Series E-ISSN 2512-2150
issn_series 2512-2142
copyrightSpringer International Publishing Switzerland 2015
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On the Mean Residual Life Regression Model,mination of IL-1-driven cascades during the proliferative phase of infarct healing may allow unopposed actions of Transforming Growth Factor (TGF)-β on cardiac fibroblasts, mediating myofibroblast transdifferentiation, matrix synthesis and scar contraction. Angiotensin II, the mast cell proteases ch
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Testing for Multivariate Distributions,fibrosis, these cells differentiate rapidly to the myofibroblast phenotype in response to injury, a process that is both facilitated and guided by microRNA. The putative role of microRNA has been implied in both the differentiation of bone marrow-derived stem cells and interstitial fibroblasts to my
发表于 2025-3-22 09:11:17 | 显示全部楼层
Heteroscedasticity Tests for Regressions,mon factors that control myofibroblast activation from different precursor cells in the heart. At least two factors are pivotal for myofibroblast activation and function: mechanical stress, manifested in disease as a stiff extracellular matrix, and active TGF-β1. Because of uncontrollable side effec
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Multivariate Kernel Estimators,endocardium, and valve progenitors within, are still not entirely elucidated. The current paradigm stipulates that endocardium is mainly derived from two early embryonic fields, the first and second heart fields. Further delineating the origins of valve progenitors and their specification towards th
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H. Büringer,H. Martin,K.-H. Schrieverrom multiple sources from the close proximity of the wound area such as from epithelial and endothelial cells via EMT and EndMT, and from circulating bone marrow progenitor cells or from fibrocytes and pericytes. Due to persistent pathological stimuli, the resulting uncontrolled proliferation of fib
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