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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Lack-of-Fit Tests Based on Linear Smoothers,anslational modification, and downstream ECM substrates. We also explore the overall important role of MMP-9 in adverse cardiac remodeling post-MI and its potential utility as a pathophysiological biomarker. Finally, we highlight MMP-9 endogenous and pharmacological inhibitors and the challenges tha

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P. Bertail,O. Jelassi,J. Tressou,M. Zetlaouiling ratio is 1:1, this concentration-dependent effect is due to ligand-gated current in the myofibroblast depolarizing the myocyte through heterotypic connexin-mediated intercellular junctions. In addition to changing the resting potential in the myocyte, the S-1-P induced current resulted in signi

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Francesca Romana Crucinio,Roberto Fontanag these is the ability to prevent fibroblast proliferation and abnormal collagen deposition in the ECM. NPs elicit their effects by binding to three NP receptors denoted NPR-A, NPR-B and NPR-C. NPR-A and NPR-B are guanylyl cyclase-linked NPRs that elicit their effects by increasing cGMP levels. NPR-

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Book 2015atrix 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

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Mechanical and Matrix Regulation of Valvular Fibrosis,x composition further influence these cellular responses. There is also abundant biochemical signaling in the aortic root, with molecular factors either produced by valve cells or transported to the root via blood flow. When these mechanical/biochemical processes become deregulated as a result of in

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