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      Current Understanding of the Pathophysiology of Myocardial Fibrosis and Its Quantitative Assessment in Heart Failure

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          Abstract

          Myocardial fibrosis is an important part of cardiac remodeling that leads to heart failure and death. Myocardial fibrosis results from increased myofibroblast activity and excessive extracellular matrix deposition. Various cells and molecules are involved in this process, providing targets for potential drug therapies. Currently, the main detection methods of myocardial fibrosis rely on serum markers, cardiac magnetic resonance imaging, and endomyocardial biopsy. This review summarizes our current knowledge regarding the pathophysiology, quantitative assessment, and novel therapeutic strategies of myocardial fibrosis.

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          Most cited references66

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          Quantifying the heart failure epidemic: prevalence, incidence rate, lifetime risk and prognosis of heart failure The Rotterdam Study.

          To determine the prevalence, incidence rate, lifetime risk and prognosis of heart failure. The Rotterdam Study is a prospective population-based cohort study in 7983 participants aged > or =55. Heart failure was defined according to criteria of the European Society of Cardiology. Prevalence was higher in men and increased with age from 0.9% in subjects aged 55-64 to 17.4% in those aged > or =85. Incidence rate of heart failure was 14.4/1000 person-years (95% CI 13.4-15.5) and was higher in men (17.6/1000 man-years, 95% CI 15.8-19.5) than in women (12.5/1000 woman-years, 95% CI 11.3-13.8). Incidence rate increased with age from 1.4/1000 person-years in those aged 55-59 to 47.4/1000 person-years in those aged > or =90. Lifetime risk was 33% for men and 29% for women at the age of 55. Survival after incident heart failure was 86% at 30 days, 63% at 1 year, 51% at 2 years and 35% at 5 years of follow-up. Prevalence and incidence rates of heart failure are high. In individuals aged 55, almost 1 in 3 will develop heart failure during their remaining lifespan. Heart failure continues to be a fatal disease, with only 35% surviving 5 years after the first diagnosis.
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            Myofibroblast-mediated mechanisms of pathological remodelling of the heart.

            The syncytium of cardiomyocytes in the heart is tethered within a matrix composed principally of type I fibrillar collagen. The matrix has diverse mechanical functions that ensure the optimal contractile efficiency of this muscular pump. In the diseased heart, cardiomyocytes are lost to necrotic cell death, and phenotypically transformed fibroblast-like cells-termed 'myofibroblasts'-are activated to initiate a 'reparative' fibrosis. The structural integrity of the myocardium is preserved by this scar tissue, although at the expense of its remodelled architecture, which has increased tissue stiffness and propensity to arrhythmias. A persisting population of activated myofibroblasts turns this fibrous tissue into a living 'secretome' that generates angiotensin II and its type 1 receptor, and fibrogenic growth factors (such as transforming growth factor-β), all of which collectively act as a signal-transducer-effector signalling pathway to type I collagen synthesis and, therefore, fibrosis. Persistent myofibroblasts, and the resultant fibrous tissue they produce, cause progressive adverse myocardial remodelling, a pathological hallmark of the failing heart irrespective of its etiologic origin. Herein, we review relevant cellular, subcellular, and molecular mechanisms integral to cardiac fibrosis and consequent remodelling of atria and ventricles with a heterogeneity in cardiomyocyte size. Signalling pathways that antagonize collagen fibrillogenesis provide novel strategies for cardioprotection.
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              MicroRNA therapeutics for cardiovascular disease: opportunities and obstacles.

              In recent years, prominent roles for microRNAs (miRNAs) have been uncovered in several cardiovascular disorders. The ability to therapeutically manipulate miRNA expression and function through systemic or local delivery of miRNA inhibitors, referred to as antimiRs, has triggered enthusiasm for miRNAs as novel therapeutic targets. Here, we focus on the pharmacokinetic and pharmacodynamic properties of current antimiR designs and their relevance to cardiovascular indications, and evaluate the opportunities and obstacles associated with this new therapeutic modality.
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                Author and article information

                Contributors
                Journal
                Front Physiol
                Front Physiol
                Front. Physiol.
                Frontiers in Physiology
                Frontiers Media S.A.
                1664-042X
                24 April 2017
                2017
                : 8
                : 238
                Affiliations
                [1] 1Department of Cardiology, Capital Medical University, Beijing AnZhen Hospital Beijing, China
                [2] 2Department of Cardiology, Beijing Changping Hospital Beijing, China
                [3] 3Department of Vascular Surgery, Chinese PLA General Hospital Beijing, China
                [4] 4Vascular Surgery Research Laboratories, Division of Vascular and Endovascular Surgery, Brigham and Women's Hospital, Harvard Medical School Boston, MA, USA
                [5] 5Department of Radiology, Beijing Anzhen Hospital, Capital Medical University Beijing, China
                [6] 6State Key Lab of Space Medicine Fundamentals and Application, China Astronaut Research and Training Center Beijing, China
                Author notes

                Edited by: Gaetano Santulli, Columbia University, USA

                Reviewed by: Carla Contaldi, Northwestern University, USA and Fatebenefratelli Hospital Benevento, Italy; Christian F. Deschepper, Institut de Recherches Cliniques de Montréal (IRCM), Canada; Jop Van Berlo, University of Minnesota, USA; Paola Matarrese, Institute for Medical Research, Malaysia

                *Correspondence: Tong Liu ltanzhen@ 123456126.com

                This article was submitted to Clinical and Translational Physiology, a section of the journal Frontiers in Physiology

                †Co-first Author.

                Article
                10.3389/fphys.2017.00238
                5402617
                28484397
                5995a76d-de91-4ca3-941d-58782468803e
                Copyright © 2017 Liu, Song, Dong, Zhu, Liu, Liu, Ma, Zhao and Ling.

                This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

                History
                : 12 January 2017
                : 05 April 2017
                Page count
                Figures: 2, Tables: 2, Equations: 0, References: 97, Pages: 13, Words: 11145
                Categories
                Physiology
                Review

                Anatomy & Physiology
                mycardial fibrosis,heart failure,late gadolinium enhancement,micro rnas (mirnas),biomarkers,extracelluar matrix

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