NDLI: The pathogenesis of cardiac fibrosis

Content Provider	Springer Nature Link
Author	Kong, Ping Christia, Panagiota Frangogiannis, Nikolaos G.
Copyright Year	2013
Abstract	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.
Starting Page	549
Ending Page	574
Page Count	26
File Format	PDF
ISSN	1420682X
Journal	Cellular and Molecular Life Sciences
Volume Number	71
Issue Number	4
e-ISSN	14209071
Language	English
Publisher	Springer Basel
Publisher Date	2013-05-07
Publisher Place	Basel
Access Restriction	Subscribed
Subject Keyword	Myofibroblast Cardiac remodeling Macrophage Mast cell Chemokine TGF-β Angiotensin Extracellular matrix Cell Biology Biomedicine general Life Sciences Biochemistry
Content Type	Text
Resource Type	Article
Subject	Cell Biology Molecular Biology Molecular Medicine Pharmacology Cellular and Molecular Neuroscience

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