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The pathogenesis of cardiac fibrosis

Cardiac fibrosis is characterized by net accumulation of extracellular matrix proteins in the cardiac interstitium, and contributes to both systolic and diastolic dysfunction in many cardiac pathophysiologic conditions. This review discusses the cellular effectors and molecular pathways implicated i... Full description

Journal Title: Cellular and molecular life sciences : CMLS 2013-05-07, Vol.71 (4), p.549-574
Main Author: Kong, Ping
Other Authors: Christia, Panagiota , Frangogiannis, Nikolaos G
Format: Electronic Article Electronic Article
Language: English
Subjects:
Publisher: Basel: Springer Basel
ID: ISSN: 1420-682X
Link: https://www.ncbi.nlm.nih.gov/pubmed/23649149
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recordid: cdi_springer_journals_10_1007_s00018_013_1349_6
title: The pathogenesis of cardiac fibrosis
format: Article
creator:
  • Kong, Ping
  • Christia, Panagiota
  • Frangogiannis, Nikolaos G
subjects:
  • Angiotensin
  • Angiotensins - immunology
  • Animals
  • Article
  • Biochemistry
  • Biomedical and Life Sciences
  • Biomedicine
  • Cardiac arrhythmia
  • Cardiac patients
  • cardiac remodeling
  • Cell Biology
  • chemokine
  • Chemokines
  • Cytokines - immunology
  • extracellular matrix
  • Fibrosis
  • Fibrosis - complications
  • Fibrosis - immunology
  • Fibrosis - pathology
  • general
  • Growth factors
  • Heart Failure - etiology
  • Heart Failure - pathology
  • Humans
  • Life Sciences
  • macrophage
  • Macrophages - immunology
  • Macrophages - pathology
  • mast cell
  • Mast Cells - immunology
  • Mast Cells - pathology
  • Matrix
  • Medical colleges
  • Myocardium - immunology
  • Myocardium - pathology
  • myofibroblast
  • Myofibroblasts - immunology
  • Myofibroblasts - pathology
  • Pathogenesis
  • Proteases
  • Proteins
  • Review
  • Signal Transduction
  • TGF-β
ispartof: Cellular and molecular life sciences : CMLS, 2013-05-07, Vol.71 (4), p.549-574
description: Cardiac fibrosis is characterized by net accumulation of extracellular matrix proteins in the cardiac interstitium, and contributes to both systolic and diastolic dysfunction in many cardiac pathophysiologic conditions. This review discusses the cellular effectors and molecular pathways implicated in the pathogenesis of cardiac fibrosis. Although activated myofibroblasts are the main effector cells in the fibrotic heart, monocytes/macrophages, lymphocytes, mast cells, vascular cells and cardiomyocytes may also contribute to the fibrotic response by secreting key fibrogenic mediators. Inflammatory cytokines and chemokines, reactive oxygen species, mast cell-derived proteases, endothelin-1, the renin/angiotensin/aldosterone system, matricellular proteins, and growth factors (such as TGF-β and PDGF) are some of the best-studied mediators implicated in cardiac fibrosis. Both experimental and clinical evidence suggests that cardiac fibrotic alterations may be reversible. Understanding the mechanisms responsible for initiation, progression, and resolution of cardiac fibrosis is crucial to design anti-fibrotic treatment strategies for patients with heart disease.
language: eng
source:
identifier: ISSN: 1420-682X
fulltext: no_fulltext
issn:
  • 1420-682X
  • 1420-9071
url: Link


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descriptionCardiac fibrosis is characterized by net accumulation of extracellular matrix proteins in the cardiac interstitium, and contributes to both systolic and diastolic dysfunction in many cardiac pathophysiologic conditions. This review discusses the cellular effectors and molecular pathways implicated in the pathogenesis of cardiac fibrosis. Although activated myofibroblasts are the main effector cells in the fibrotic heart, monocytes/macrophages, lymphocytes, mast cells, vascular cells and cardiomyocytes may also contribute to the fibrotic response by secreting key fibrogenic mediators. Inflammatory cytokines and chemokines, reactive oxygen species, mast cell-derived proteases, endothelin-1, the renin/angiotensin/aldosterone system, matricellular proteins, and growth factors (such as TGF-β and PDGF) are some of the best-studied mediators implicated in cardiac fibrosis. Both experimental and clinical evidence suggests that cardiac fibrotic alterations may be reversible. Understanding the mechanisms responsible for initiation, progression, and resolution of cardiac fibrosis is crucial to design anti-fibrotic treatment strategies for patients with heart disease.
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subjectAngiotensin ; Angiotensins - immunology ; Animals ; Article ; Biochemistry ; Biomedical and Life Sciences ; Biomedicine ; Cardiac arrhythmia ; Cardiac patients ; cardiac remodeling ; Cell Biology ; chemokine ; Chemokines ; Cytokines - immunology ; extracellular matrix ; Fibrosis ; Fibrosis - complications ; Fibrosis - immunology ; Fibrosis - pathology ; general ; Growth factors ; Heart Failure - etiology ; Heart Failure - pathology ; Humans ; Life Sciences ; macrophage ; Macrophages - immunology ; Macrophages - pathology ; mast cell ; Mast Cells - immunology ; Mast Cells - pathology ; Matrix ; Medical colleges ; Myocardium - immunology ; Myocardium - pathology ; myofibroblast ; Myofibroblasts - immunology ; Myofibroblasts - pathology ; Pathogenesis ; Proteases ; Proteins ; Review ; Signal Transduction ; TGF-β
ispartofCellular and molecular life sciences : CMLS, 2013-05-07, Vol.71 (4), p.549-574
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descriptionCardiac fibrosis is characterized by net accumulation of extracellular matrix proteins in the cardiac interstitium, and contributes to both systolic and diastolic dysfunction in many cardiac pathophysiologic conditions. This review discusses the cellular effectors and molecular pathways implicated in the pathogenesis of cardiac fibrosis. Although activated myofibroblasts are the main effector cells in the fibrotic heart, monocytes/macrophages, lymphocytes, mast cells, vascular cells and cardiomyocytes may also contribute to the fibrotic response by secreting key fibrogenic mediators. Inflammatory cytokines and chemokines, reactive oxygen species, mast cell-derived proteases, endothelin-1, the renin/angiotensin/aldosterone system, matricellular proteins, and growth factors (such as TGF-β and PDGF) are some of the best-studied mediators implicated in cardiac fibrosis. Both experimental and clinical evidence suggests that cardiac fibrotic alterations may be reversible. Understanding the mechanisms responsible for initiation, progression, and resolution of cardiac fibrosis is crucial to design anti-fibrotic treatment strategies for patients with heart disease.
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abstractCardiac fibrosis is characterized by net accumulation of extracellular matrix proteins in the cardiac interstitium, and contributes to both systolic and diastolic dysfunction in many cardiac pathophysiologic conditions. This review discusses the cellular effectors and molecular pathways implicated in the pathogenesis of cardiac fibrosis. Although activated myofibroblasts are the main effector cells in the fibrotic heart, monocytes/macrophages, lymphocytes, mast cells, vascular cells and cardiomyocytes may also contribute to the fibrotic response by secreting key fibrogenic mediators. Inflammatory cytokines and chemokines, reactive oxygen species, mast cell-derived proteases, endothelin-1, the renin/angiotensin/aldosterone system, matricellular proteins, and growth factors (such as TGF-β and PDGF) are some of the best-studied mediators implicated in cardiac fibrosis. Both experimental and clinical evidence suggests that cardiac fibrotic alterations may be reversible. Understanding the mechanisms responsible for initiation, progression, and resolution of cardiac fibrosis is crucial to design anti-fibrotic treatment strategies for patients with heart disease.
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