標(biāo)題: Titlebook: Cardiac Fibrosis and Heart Failure: Cause or Effect?; Ian M.C. Dixon,Jeffrey T. Wigle Book 2015 Springer International Publishing Switzerl [打印本頁] 作者: Defect 時間: 2025-3-21 19:00
書目名稱Cardiac Fibrosis and Heart Failure: Cause or Effect?影響因子(影響力)
書目名稱Cardiac Fibrosis and Heart Failure: Cause or Effect?影響因子(影響力)學(xué)科排名
書目名稱Cardiac Fibrosis and Heart Failure: Cause or Effect?網(wǎng)絡(luò)公開度
書目名稱Cardiac Fibrosis and Heart Failure: Cause or Effect?網(wǎng)絡(luò)公開度學(xué)科排名
書目名稱Cardiac Fibrosis and Heart Failure: Cause or Effect?被引頻次
書目名稱Cardiac Fibrosis and Heart Failure: Cause or Effect?被引頻次學(xué)科排名
書目名稱Cardiac Fibrosis and Heart Failure: Cause or Effect?年度引用
書目名稱Cardiac Fibrosis and Heart Failure: Cause or Effect?年度引用學(xué)科排名
書目名稱Cardiac Fibrosis and Heart Failure: Cause or Effect?讀者反饋
書目名稱Cardiac Fibrosis and Heart Failure: Cause or Effect?讀者反饋學(xué)科排名
作者: 黑豹 時間: 2025-3-21 23:51
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作者: Lament 時間: 2025-3-22 03:19 作者: ostracize 時間: 2025-3-22 06:29
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作者: Axillary 時間: 2025-3-22 09:11
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作者: 相互影響 時間: 2025-3-22 16:40
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作者: 相互影響 時間: 2025-3-22 18:40
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作者: morale 時間: 2025-3-22 21:52 作者: FOVEA 時間: 2025-3-23 02:09 作者: 同步左右 時間: 2025-3-23 06:04 作者: 名義上 時間: 2025-3-23 11:09
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作者: Desert 時間: 2025-3-23 14:03 作者: 密碼 時間: 2025-3-23 20:32 作者: 執(zhí)拗 時間: 2025-3-23 22:39
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作者: 切碎 時間: 2025-3-24 03:33 作者: Encephalitis 時間: 2025-3-24 10:15
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-作者: Rheumatologist 時間: 2025-3-24 12:19
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作者: insightful 時間: 2025-3-24 15:35 作者: Esalate 時間: 2025-3-24 22:07
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作者: Working-Memory 時間: 2025-3-25 02:44 作者: caldron 時間: 2025-3-25 07:05 作者: 只有 時間: 2025-3-25 10:29
Embryological Origin of Valve Progenitor Cells,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作者: 窗簾等 時間: 2025-3-25 12:49 作者: Coma704 時間: 2025-3-25 18:19 作者: 天氣 時間: 2025-3-25 20:59 作者: 收集 時間: 2025-3-26 00:44
Remodelling of the Cardiac Extracellular Matrix: Role of Collagen Degradation and Accumulation in Pon resulting in an uncoupling between collagen mRNA and protein levels. In this chapter, we will provide an overview of the mechanisms involved in myocardial fibrosis, the disease-dependent nature and consequence of different types of fibrosis, clinical biomarkers of collagen turnover, and potential作者: infantile 時間: 2025-3-26 05:06
Matrix Metalloproteinase 9 (MMP-9),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作者: CBC471 時間: 2025-3-26 11:49 作者: Traumatic-Grief 時間: 2025-3-26 14:23 作者: 陳腐思想 時間: 2025-3-26 18:11 作者: insert 時間: 2025-3-27 00:17 作者: dialect 時間: 2025-3-27 03:04
Natriuretic Peptides: Critical Regulators of Cardiac Fibroblasts and the Extracellular Matrix in thg 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-作者: Bombast 時間: 2025-3-27 09:22
Cardiac Fibrosis and Heart Failure: Cause or Effect?作者: 減至最低 時間: 2025-3-27 13:27 作者: GREEN 時間: 2025-3-27 16:49
978-3-319-37995-1Springer International Publishing Switzerland 2015作者: Outwit 時間: 2025-3-27 21:40
Cardiac Fibrosis and Heart Failure: Cause or Effect?978-3-319-17437-2Series ISSN 2512-2142 Series E-ISSN 2512-2150 作者: 主動 時間: 2025-3-28 00:44 作者: 一條卷發(fā) 時間: 2025-3-28 02:55
Homegeneity Testing for Covariance Matrices,recent advances in our understanding have allowed us to identify cardiac fibrosis as a primary disease independent of either cardiomyocyte injury or loss. New developments within this field are burgeoning, including research that points to multiple sources for cardiac myofibroblasts participating in作者: 芭蕾舞女演員 時間: 2025-3-28 09:55 作者: capsaicin 時間: 2025-3-28 13:44
https://doi.org/10.1007/0-387-29053-2ronment results in multiple homeostatic mechanisms, but also a wide variety of putative disease pathways by which valve function can be compromised. Aortic valve disease (AVD) is a cell-mediated pathology whose initial stages are characterized by unchecked matrix dysregulation, leaflet thickening, a作者: 籠子 時間: 2025-3-28 16:53
Testing for Multivariate Distributions, and lead to heart failure. Classically thought to be the result of myofibroblasts activated from interstitial fibroblasts endogenously present within the heart, recent research has found that there are numerous cell sources contributing to fibrosis, including various stem cell lineages found in the作者: 預(yù)防注射 時間: 2025-3-28 22:17
Heteroscedasticity Tests for Regressions,o mechanical load, such as in conditions of hypertension and to repair injuries after myocardial infarct. Aberrant mechanosensing and/or persistent stress results in the chronic activation of cardiac fibroblasts and other progenitors into myofibroblasts. Myofibroblasts drive the development of fibro作者: linguistics 時間: 2025-3-29 01:38
Multivariate Kernel Estimators,de: widely scattered microscopic scars which have replaced myocytes lost to necrosis; and a perivascular fibrosis of intramural coronary arteries. An animal model of aldosterone/salt treatment has been used to examine the pathogenic origins of myocyte necrosis and coronary vasculopathy. A common cel作者: profligate 時間: 2025-3-29 05:14 作者: cortisol 時間: 2025-3-29 08:14 作者: Oligarchy 時間: 2025-3-29 14:28
H. Büringer,H. Martin,K.-H. Schrievere form of CVD. Despite the vast diversity of CVD forms, many disease states are associated with maladaptive remodeling of the myocardial interstitium. Elevated fibrillar collagen expression is considered to be the primary contributor to altered cardiac function based on its adverse influence on elec作者: NATAL 時間: 2025-3-29 18:10
H. Büringer,H. Martin,K.-H. Schriever the heart. Cardiac hypertrophy is characterized by enlargement of the heart as a result of an increase in cardiomyocyte size and also enhanced fibrosis due primarily to phenotypic conversion of fibroblasts to myofibroblasts. Also, atherosclerosis, a disease characterized by formation of plaque with作者: 控制 時間: 2025-3-29 22:54
https://doi.org/10.1007/978-1-4684-0538-5trix components including fibrillar collagen types I and III. Increased collagen synthesis and cross-linking strengthens the myocardium but also increases wall stiffness and thereby negatively impact both diastolic (filling) and systolic (contractile) function. Myocardial fibrosis occurs secondary t作者: 殺死 時間: 2025-3-30 02:25 作者: cardiac-arrest 時間: 2025-3-30 06:52
Lack-of-Fit Tests Based on Linear Smoothers,dely investigated MMPs. MMP-9 functions primarily by directly degrading and activating ECM structural and non-structural molecules to regulate cardiac tissue remodeling. This activity is opposed under physiological conditions by a set of endogenous inhibitors known as tissue inhibitors of metallopro作者: 分開 時間: 2025-3-30 08:37 作者: 不出名 時間: 2025-3-30 16:08 作者: Countermand 時間: 2025-3-30 17:40 作者: ADORE 時間: 2025-3-30 23:22 作者: 寒冷 時間: 2025-3-31 01:46
https://doi.org/10.1007/978-3-319-96941-1lem. Heart failure is the most frequent cause of hospitalization in persons 65 years of age or older and heart failure continues to impose a substantial healthcare burden, despite recent treatment advances. From both an economical and clinical perspective, there is clearly an urgent need for advance作者: abnegate 時間: 2025-3-31 09:05
Francesca Romana Crucinio,Roberto Fontana in the heart including the synthesis and remodeling of the extracellular matrix (ECM), which is the component of the heart that includes interstitial collagens. In the setting of heart disease, including heart failure (HF), abnormal fibroblast proliferation and deposition of collagens leads to adve作者: Facet-Joints 時間: 2025-3-31 12:53
Ian M.C. Dixon,Jeffrey T. WigleFocuses 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.作者: CBC471 時間: 2025-3-31 13:50 作者: consolidate 時間: 2025-3-31 20:16 作者: SPASM 時間: 2025-3-31 22:31
Homegeneity Testing for Covariance Matrices, the current state of investigation to address the biology of cardiovascular fibroblasts, valvular interstitial cells (VICs), and myofibroblasts is warranted. This book will help to adapt the information that we have gathered in order to translate it into treatments for fibrotic cardiac diseases and thus alter the course of their progression.作者: prostatitis 時間: 2025-4-1 03:52
H. Büringer,H. Martin,K.-H. Schriever describe a potential role for the TGF-β. negative regulators Ski/Sno, and the TGF-β. transcriptional regulators YAP/TAZ in cardiac fibroblast and myofibroblast phenotype and function through modulation of TGF-β. signaling.”作者: Recess 時間: 2025-4-1 07:07 作者: Asymptomatic 時間: 2025-4-1 14:13
,Non-Canonical Regulation of TGF-β1 Signaling: A Role for Ski/Sno and YAP/TAZ, describe a potential role for the TGF-β. negative regulators Ski/Sno, and the TGF-β. transcriptional regulators YAP/TAZ in cardiac fibroblast and myofibroblast phenotype and function through modulation of TGF-β. signaling.”作者: decipher 時間: 2025-4-1 15:52 作者: definition 時間: 2025-4-1 19:37 作者: 放棄 時間: 2025-4-2 02:20
