Document Detail


Wound-associated skin fibrosis: mechanisms and treatments based on modulating the inflammatory response.
MedLine Citation:
PMID:  20923404     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Skin fibrosis, in its mildest form, may present only a minor aesthetic problem, but in the most severe cases it can lead to debilitating pathologies of the skin, for example keloid and hypertrophic scars, and systemic sclerosis. In recent years, extensive basic research aimed at understanding the molecular mechanisms underlying fibrosis has revealed an impressive but baffling number of genes, molecules, and cell types that may contribute to this problem. However, one recurring and consistent theme in these studies is that inflammatory cells and their secreted mediators appear to be leading culprits in activating dermal fibroblasts to become fibrotic. This review will first describe the histology of normal versus fibrotic skin, and will also describe the process of wound repair, a primary cause of skin fibrosis. We will then focus on what is currently known about the molecular mechanisms underlying skin fibrosis, with particular attention paid to how inflammation contributes. Finally, current treatment strategies and emerging therapeutic targets will be discussed.
Authors:
Tanya J Shaw; Kazuo Kishi; Ryoichi Mori
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Review    
Journal Detail:
Title:  Endocrine, metabolic & immune disorders drug targets     Volume:  10     ISSN:  2212-3873     ISO Abbreviation:  Endocr Metab Immune Disord Drug Targets     Publication Date:  2010 Dec 
Date Detail:
Created Date:  2011-01-10     Completed Date:  2011-04-18     Revised Date:  2012-04-19    
Medline Journal Info:
Nlm Unique ID:  101269157     Medline TA:  Endocr Metab Immune Disord Drug Targets     Country:  United Arab Emirates    
Other Details:
Languages:  eng     Pagination:  320-30     Citation Subset:  IM    
Affiliation:
St George's, University of London, UK. tshaw@sgul.ac.uk
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MeSH Terms
Descriptor/Qualifier:
Animals
Cicatrix / genetics,  immunology,  pathology*,  prevention & control
Fibroblasts / immunology,  pathology
Fibrosis
Humans
Inflammation Mediators / metabolism*
Signal Transduction* / genetics
Skin / immunology,  pathology*
Wound Healing* / genetics
Chemical
Reg. No./Substance:
0/Inflammation Mediators

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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