Download or read book Matrix Metalloproteinases in Left Ventricular Remodeling written by Mytsi L. Coker and published by . This book was released on 2000 with total page 304 pages. Available in PDF, EPUB and Kindle. Book excerpt:

Download or read book Ventricular Remodeling written by Amanda L. Chancey and published by . This book was released on 2004 with total page 324 pages. Available in PDF, EPUB and Kindle. Book excerpt:

Download or read book Cardiac Remodeling written by Bodh I. Jugdutt and published by Springer Science & Business Media. This book was released on 2013-02-15 with total page 566 pages. Available in PDF, EPUB and Kindle. Book excerpt: The main objective of Cardiac Remodeling: Molecular Mechanisms is to summarize the major research advances in molecular, biochemical and translational aspects of cardiac remodeling over the last 2 to 3 decades under one cover and touch on future directions. It provides a high profile and valuable publication resource on molecular mechanisms of cardiac remodeling for both the present and future generations of researchers, teachers, students and trainees. This book should stimulate future translational research targeted towards discovery and development for preventing, limiting and reversing bad remodeling over the next few decades, with the ultimate goal of preventing progression to systolic and/or diastolic heart failure. The chapters suggest potential novel strategies that should receive attention for translating basic research knowledge to application in patients at the bedside.

Download or read book Matrix Metalloproteinases and Tissue Remodeling in Health and Disease Cardiovascular Remodeling written by and published by Academic Press. This book was released on 2017-04-14 with total page 322 pages. Available in PDF, EPUB and Kindle. Book excerpt: Matrix Metalloproteinases and Tissue Remodeling in Health and Disease: Cardiovascular Remodeling, Volume 147 contains up-to-date information on the biology and function of matrix metalloproteinases and how their effects on tissue remodeling are altered in diseases of the cardiovascular, pulmonary, and musculoskeletal systems and in other tissues and organs, and in cancer. This latest release covers such highly evolving topics as Biochemical and Biological Attributes of Matrix Metalloproteinases, Matrix Metalloproteinases in Myocardial Infarction and Heart Failure, The Balance Between Metalloproteinases and TIMPs: Critical Regulator of Microvascular Endothelial Cell Function in Health and Disease, and Matrix Metalloproteinases and Platelet Function. As part of the Progress in Molecular Biology and Translational Science, users will find contributions from prominent scientists and highly-recognized experts who have major accomplishments in the research field of matrix metalloproteinases. Focuses on matrix metalloproteinases and their role in tissue remodeling under physiological and pathological conditions Contains up-to-date information on matrix metalloproteinases that is clearly presented in a concise fashion with helpful illustrations and supporting references Includes comprehensive reviews written by prominent scientists and highly-recognized experts in the field of matrix metalloproteinases and tissue remodeling

Download or read book Matrix Metalloproteinases in Tissue Remodelling and Inflammation written by Vincent Lagente and published by Springer Science & Business Media. This book was released on 2008-11-07 with total page 177 pages. Available in PDF, EPUB and Kindle. Book excerpt: This volume provides new advances regarding the involvement of MMPs in various diseases associated with inflammatory processes. Moreover, the recent development of selective and non selective inhibitors of MMPs give new insights in the relationship between activation of inflammatory cells and tissue remodelling and advise new therapeutics possibilities to the treatment of inflammatory disease. The volume has an international authorship and is written by leading experts in the field.

Download or read book Plasma Matrix Metalloproteinases as Predictors of Prognosis and Left Ventricular Remodelling After Acute Myocardial Infarction written by Dominic Kelly and published by . This book was released on 2008 with total page pages. Available in PDF, EPUB and Kindle. Book excerpt: Introduction: Matrix metalloproteinases (MMPs) are a family ofzinc dependant endopeptidases which selectively degrade components ofthe extracellular matrix. Degradation ofthis matrix is central to several aspects ofcardiovascular disease including adverse left ventricular remodelling, a process which is intimately linked to prognosis. The basis ofthis thesis was to investigate the role ofMMP's and their natural inhibitors tissue inhibitors ofmetalloproteinases (T!MP's) in the process of left ventricular remodelling, clinical heart failure and adverse prognosis post acute myocardial infarction (AMI). Methods: We recruited patients post AMI. Stage I aimed to examine the temporal profile of several MMP's and their relationship with markers ofLV function, volumes and remodelling in a limited population size (n=9I). Stage 2 investigated a more extensive population (n=404), concentrating on a limited number ofMMP's/TIMP's and included clinical follow up to identify subjects with adverse prognosis. All patients were recruited from the CCU units ofthe University Hospitals ofLeicester. All donated venous blood samples at 0-12hrs, 12-24hrs and at 24hr intervals post symptoms until discharge for measurement ofMMP/TIMP's and underwent echocardiographic studies during their index admission and at follow up. During stage 2 all subjects were additionally followed for the clinical endpoints ofdeath or heart failure. We also performed a retrospective analysis ofthe effects ofdiabetes and stress hyperglycaemia on metalloproteinase expression and LV dysfunction post MI. Results: We present convincing data to implicate the MMP system in both LV remodelling and adverse prognosis post AMI. Stage I demonstrates individual temporal profiles of MMP's and presents data on determinants ofMMP expression. We show an association between MMP-9 and LV dysfunction, volumes and remodelling post AMI. Stage 2 confirms both this data and observes similar results for TIMP-I. In addition we demonstrate the association between both MMP-9 and TIMP-I with adverse prognosis and compare with N terminal pro BNP as a prognostic marker. Our retrospective audit ofthe effects ofdiabetes and stress hyperglycaemia is a hypothesis generating chapter which presents association between post MI hyperglycaemia, elevated MMP's and adverse LV function. Summary: Altered MMP/TIMP expression occurs post AMI and is associated with LV dysfunction and remodelling, and with adverse prognosis. The MMP system may represent a potential therapeutic target post AMI.

Download or read book The Role of Matrix Metalloproteinases Induced Angiogenesis During Transition from Compensatory Cardiac Hypertrophy to Cardiac Failure written by Srikanth Givvimani and published by . This book was released on 2010 with total page 280 pages. Available in PDF, EPUB and Kindle. Book excerpt: Background: Although matrix metalloproteinase (MMPs) and tissue inhibitor of metalloproteinase (TIMPs) play a vital role in tumor angiogenesis and TIMP-3 causes apoptosis, their role in cardiac angiogenesis is unknown. Interestingly, a disruption of coordinated cardiac hypertrophy and angiogenesis contributes to the transition to heart failure, however, the proteolytic and anti-angiogenic mechanisms of transition from compensatory hypertrophy to decompensatory heart failure are unclear. Previous studies have shown the cardio protective role of hydrogen sulfide (H2S) in myocardial ischemia, infarction and heart failure, but its role during transition from compensatory cardiac hypertrophy to heart failure is yet to be unveiled. We hypothesize that in pathological pressure overload of the heart, cardiac matrix remodeling is induced by an increase in angiogenic growth factors during the compensatory hypertrophy phase and an increase in antiangiogenic factors during the decompensatory heart failure phase. H2S mitigates the transition from compensatory hypertrophy to decompensatory heart failure by increasing angiogenesis and decreasing fibrosis. Methods: In the first set of experiments, we have created ascending aortic banding (AB) in the mice to mimic pressure overload on the heart and studied the ventricular remodeling events associated with chronic pressure overload. Male wild type mice were used and all animal procedures were performed in accordance with National Institute of Health guidelines for animal research and were reviewed and approved by the Institute Animal Care and use Committee of University of Louisville. Sham animals underwent similar procedures except for aortic banding. Animals were studied at 3 weeks (compensatory phase) and 8 weeks period (decompensatory phase) and compared with sham groups. In the second set of experiment, similar protocol was followed, and animals were treated with hydrogen sulfide (H2S) for 6 weeks by giving sodium hydrosulfide (NaHS) in drinking water and compared with untreated groups. Molecular and functional data were assessed by echocardiography, pressure-volume (P-V) study, immunohistochemistry, histology, western blot, and x-ray angiography. Results: We found that in the first set of experiments, expression of MMP-2 increased along with angiogenic growth factor, vascular endothelial growth factor (VEGF) during compensatory phase (AB 3 weeks group). Expression of MMP-9, TIMP-3 and anti-angiogenic factors, angiostatin, and endostatin increased during decompensatory phase (AB 8 weeks group). There was increased deposition of fibrosis during the decompensatory phase. By treating with H2S, we noticed that there was increased expression of VEGF and MMP-2 in AS 8 weeks group than in untreated AS 8 weeks group. Interestingly, the expression of MMP-9, TIMP-3 and anti-angiogenic factors angiostatin and endostatin decreased in H2S treated AS 8 weeks group than in the untreated group. There was significant reduction of fibrosis in treated AS 8 weeks group. Left ventricular function also improved in H2S treated AS 8 weeks group. Conclusion: we conclude that under chronic pressure overload, expression of MMP-2 is induced which in turn increases the release of angiogenic growth factors in compensatory cardiac hypertrophy. The expression of MMP-9 and TIMP-3 is also increased leading to a release of anti-angiogenic factors in decompensatory heart failure. Hydrogen sulfide mitigates this transition to decompensatory heart failure not only by inducing MMP-2NEGF but also inhibiting MMP-9/TIMP-3 and anti-angiogenic factors.

Download or read book Matrix Metalloproteinases and TIMPs written by J. F. Woessner and published by Oxford University Press on Demand. This book was released on 2000 with total page 223 pages. Available in PDF, EPUB and Kindle. Book excerpt: The matrix metalloproteinases (MMPs) are a large family of enzymes that breakdown different components of the extracellular matrix. Their catalytic activity is dependent a metal ion, usually zinc. This issue of the Protein Profiles covers the sequence information, three-dimensional structures, activation, protein substrates, specificity requirements, inhibition, and biological roles of all the currently identified MMPs. The action of these enzymes must be carefully regulated. One way the cell does this, is by releasing inhibitory molecules known as tissue inhibitors of metalloproteinases (TIMPs). This volume contains information on the sequences, three-dimensional structures, and biological roles of the 4 known classes of TIMP. Matrix metalloproteinases will therefore be an invaluable source of data for all researchers interested in MMPs and TIMPs.

Download or read book Mechanisms of Cardiac Remodeling and Failure microform Role of the Tissue Inhibitor of Matrix Metalloproteinase 3 written by Paul William Michael Fedak and published by Library and Archives Canada = Bibliothèque et Archives Canada. This book was released on 2004 with total page 470 pages. Available in PDF, EPUB and Kindle. Book excerpt: TIMPs (tissue inhibitors of metalloproteinases) are complex endogenous biomolecules that contribute to the regulation of tissue architecture and remodeling in both health and disease. Of the four TIMP species, TIMP-3 is unique and its role in the adult heart is undefined. We hypothesized that TIMP-3 plays a key role in initiating, coordinating, and maintaining maladaptive cardiac remodeling in the failing heart. To establish a proof-of-concept that TIMP-3 influences myocardial remodeling and dysfunction, mutant mice lacking TIMP-3 by gene deletion were assessed for altered cardiac structure and function with aging. Cardiomyopathic human and hamster myocardium was similarly assessed for architectural, cellular, and molecular indices of maladaptive remodeling in relation to TIMP-3 expression. The profile of TIMP expression was then assessed in vascular smooth muscle cell-transplanted cardiomyopathic hamster hearts to identify a mechanism through which cell transplantation limits the progression of heart failure. TIMP-3 gene deletion in mice triggered progressive cardiac dilatation and dysfunction consistent with human dilated cardiomyopathy. At the cellular level, loss of TIMP-3 expression resulted in profound cardiac matrix disruption and cell death. At the molecular level, loss of TIMP-3 activated matrix metalloproteinase-9 and the pro-inflammatory TNF-alpha cytokine system. TIMP-3 was reduced in both human and dilated cardiomyopathic hamster myocardium in association with maladaptive cardiac remodeling. In hamster cardiomyopathy, cell transplantation partially restored deficient TIMP-3 and limited maladaptive matrix remodeling. These results suggest that TIMP-3 directly influences matrix homeostasis and cytokine bioactivation in the heart. Altered TIMP-3 expression in the failing heart may directly contribute to maladaptive myocardial tissue remodeling, cardiac dysfunction, and the progression to heart failure. Replacement of deficient TIMP-3 by gene or cell therapy may provide a novel approach to prevent disease progression in patients at risk of heart failure.

Download or read book Dilated Cardiomyopathy written by Gianfranco Sinagra and published by Springer. This book was released on 2019-05-17 with total page 241 pages. Available in PDF, EPUB and Kindle. Book excerpt: This open access book presents a comprehensive overview of dilated cardiomyopathy, providing readers with practical guidelines for its clinical management. The first part of the book analyzes in detail the disease’s pathophysiology, its diagnostic work up as well as the prognostic stratification, and illustrates the role of genetics and gene-environment interaction. The second part presents current and future treatment options, highlighting the importance of long-term and individualized treatments and follow-up. Furthermore, it discusses open issues, such as the apparent healing phenomenon, the early prognosis of arrhythmic events or the use of genetic testing in clinical practice. Offering a multidisciplinary approach for optimizing the clinical management of DCM, this book is an invaluable aid not only for the clinical cardiologists, but for all physicians involved in the care of this challenging disease.

Download or read book Metalloproteinases in the Development of Hypertension and Cardiac Remodeling written by Xiang Wang and published by . This book was released on 2013 with total page 322 pages. Available in PDF, EPUB and Kindle. Book excerpt: Despite many decades of research and drug development, the diseases of the cardiovascular system remain a major health threat in the modern world. Hypertensive cardiac disease is a cardiovascular condition characterized by the co-occurrence of hypertension and pathological cardiac remodeling (hypertrophy and fibrosis). Causative factors of hypertensive cardiac disease range from environmental stress to metabolic morbidities. However, these detrimental factors have a common effector mechanism: the sustained activation of G protein-coupled receptors (GPCRs) due to pathological levels of cognate agonists which elevate systemic blood pressure and promote pathological cardiovascular remodeling. GPCR agonists can trigger the activation of metalloproteinases, including matrix metalloproteinases (MMPs) and a disintegrin and metalloproteinases (ADAMs). These metalloproteinases are multifunctional enzymes that transactivate many intracellular signaling pathways including those leading to hypertension and cardiac remodeling. Therefore, MMPs and ADAMs have been widely speculated to be potential treatment targets for hypertensive cardiac disease. In the current studies, we use angiotensin II and adrenoceptor ligands as prototypes of GPCR agonists to gain insights into mechanisms of hypertensive heart disease in rodent models. We determine various new roles played by MMP-2, MMP-7, ADAM-12 and ADAM-17. We demonstrate that: 1. MMP-7 mediates GPCR agonist-induced signaling with MMP-7 inhibition by pharmacological blockade, RNA interference or genetic knockout protecting against hypertensive cardiac remodeling. 2. ADAM-17 also contributes to GPCR agonist-induced cardiac hypertrophy and fibrosis. These effects of ADAM-17 are signaledby ADAM-12, a major effector metalloproteinase in cardiac hypertrophy signaling. 3. MMP-2 contributes to the development of GPCR agonist-induced hypertension such that partial blockade of MMP-2 by inhibitors and RNA interference attenuates angiotensin II-induced hypertension. 4. MMP-2 protects against hypertensive cardiac remodeling. To explain the cardioprotection rendered by MMP-2, we evoke a novel mechanism of negative regulation of the sterol-regulatory element binding protein (SREBP)-2 / 3-hydroxy-3-methyl-glutaryl-CoA reductase (HMGCR) pathway of cardiac remodeling. These findings are a major contribution to our current understanding of the cardiovascular biology of metalloproteinases. Our data show the diverse roles of metalloproteinases in hypertensive cardiac disease and the potential and limitations of therapeutic approaches based on metalloproteinase inhibition for management of cardiovascular disease.

Download or read book Matrix Metalloproteinase 13 Regulates Cardiac Remodeling and Inflammation After Myocardial Infarction written by Vivien Iris Lang and published by . This book was released on 2018 with total page pages. Available in PDF, EPUB and Kindle. Book excerpt:

Download or read book The Effect of Matrix Metalloproteinase Inhibition on Post myocardial Infarction Cardiac Function Remodeling and Gene Expression microform written by Jonathan Eliot Adam and published by Library and Archives Canada = Bibliothèque et Archives Canada. This book was released on 2005 with total page 190 pages. Available in PDF, EPUB and Kindle. Book excerpt: Background. Myocardial infarction (MI) is associated with ventricular hypertrophy and poorer survival. Matrix-metalloproteinases inhibition (M) has been implicated in post-MI remodeling. Methodology. Rat model, angiotensin-converting enzyme inhibitor (A) and M were administered [both(A/M); neither( -/- ); alone(A/-, -/M)] to both MI and Sham (Sh) operated rats. Function assessed by Langendorff apparatus and echocardiography, remodeling by echocardiograms and H & E slides, collagen by Picosirius-red staining. DNA microarray analysis to determine changes in gene expression. Results. All data: Sh( -/- ), MI( -/- ), MI( -/M). Langendorff developed pressure, positive and negative dP/dT demonstrated similar trends. Statistics: significant difference (P & lt; 0.05) between Sh( -/- ) and MI( -/M) and between MI( -/- ) and MI( -/M) and no significance between Sh( -/- ) and MI( -/- ) for any parameters. Echocardiography (function and morphometry), H & E morphometry and collagen: P & lt; 0.05 between MI and Sh but no difference between drug treatments. Microarray: altered gene expression classified in areas of apoptosis, anti-inflammatory, structural and novel. Conclusion. The results suggest similar improvements with both A and M on MI hearts.

Download or read book The Role of Matrix Metalloproteinase in Human Body Pathologies written by Francesco Travascio and published by BoD – Books on Demand. This book was released on 2017-12-20 with total page 202 pages. Available in PDF, EPUB and Kindle. Book excerpt: Matrix metalloproteinases (MMPs) are a family of proteolytic zinc-containing enzymes involved in physiological as well as in pathological processes in the human organism. MMPs play a key role in the remodeling of the extracellular matrix. Such a process may occur because of tissue homeostasis, morphogenesis, and tissue repair. However, remodeling could also be a part of many pathological states such as arthritis, cardiovascular diseases, neurodegenerative diseases, or impaired development in congenital anomalies. This book overviews the role of MMPs in different pathologies affecting the human body.

Download or read book Proteases in Human Diseases written by Sajal Chakraborti and published by Springer. This book was released on 2017-07-13 with total page 516 pages. Available in PDF, EPUB and Kindle. Book excerpt: This book bridges the gap between fundamental research and biomedical and pharmacological applications on proteases. It represents a comprehensive overview of the multifaceted field of proteases in cellular environment and highlights the recently elucidated functions of complex proteolytic systems in different diseases. Several established investigators have elucidated the crucial role of proteases in biological processes, including how proteolytic function and regulation can be combined to develop new strategies of therapeutic interventions. Proteases form one of the largest and most diverse families of enzymes known. It is now clear that proteases are involved in every aspect of life functions of an organism. Under physiological conditions, proteases are regulated by their endogenous inhibitors; however, when the activity of proteases is not regulated appropriately, disease processes can result in. So, there is absolute need for a stringent control of proteolytic activities in cells and tissues. Dysregulation of proteases may cause derangement of cellular signalling network resulting in different pathophysiological conditions such as vascular remodelling, atherosclerotic plaque progression, ulcer and rheumatoid arthritis, Alzheimer disease, cancer metastasis, tumor progression and inflammation. Additionally, many infective microorganisms require proteases for replication or use proteases as virulence factors, which have facilitated the development of protease-targeted therapies for a variety of parasitic diseases.

Download or read book Cardiac CT PET and MR written by Vasken Dilsizian and published by John Wiley & Sons. This book was released on 2011-09-14 with total page 525 pages. Available in PDF, EPUB and Kindle. Book excerpt: This careful revision keeps pace with developments in the field, with new chapters on PET Metabolism, CT and MRI in the Emergency Department, Image-Guided Electrophysiology Mapping and Ablation, and Identification of Vulnerable Atherosclerotic Plaque by Radionuclide and CT techniques, plus the introduction of new contributors Udo Hoffman and Stephan Achenbach. Praised in its previous edition as a concise source of essential information, this new edition presents the most recent information in an accessible format and serves as an excellent reference source for all cardiologists, radiologists and nuclear medicine physicians.

Download or read book Matrix Metalloproteinases and Tissue Remodeling in Health and Disease Target Tissues and Therapy written by and published by Academic Press. This book was released on 2017-06-26 with total page 0 pages. Available in PDF, EPUB and Kindle. Book excerpt: Matrix Metalloproteinases and Tissue Remodeling in Health and Disease: Target Tissues and Therapy, Volume, Volume 148, the latest volume in the Progress in Molecular Biology and Translational Science series covers a variety of timely topics, with chapters focusing on The Role of Matrix Metalloproteinases in Development, Repair, and Destruction of the Lungs, Matrix Metalloproteinases in Kidney Disease: Role in Pathogenesis and Potential as a Therapeutic Target, Regulation of Matrix Metalloproteinase in the Pathogenesis of Diabetic Retinopathy, Matrix Metalloproteinases in Normal Pregnancy and Preeclampsia, and Matrix Metalloproteinases, Neural Extracellular Matrix, and Central Nervous System Pathology. This volume is the second part of a thematic on matrix metalloproteinases and tissue remodeling in health and disease. It focuses on the role of MMPs in other systems, target tissues, and pathological disorders and the potential benefits of MMP inhibitors in various disorders.