Document Detail

The pro-inflammatory environment in recalcitrant diabetic foot wounds.
MedLine Citation:
PMID:  19006574     Owner:  NLM     Status:  MEDLINE    
Lower extremity ulceration is one of the serious and long-term diabetic complications rendering a significant social burden in terms of amputation and quality-of-life reduction. Diabetic patients experience a substantial wound-healing deficit. These lesions are featured by an exaggerated and prolonged inflammatory reaction with a significant impairment in local bacterial invasion control. Experimental and clinical evidences document the deleterious consequences of the wound's pro-inflammatory phenotype for the repair process. From a biochemical standpoint, hyperinflammation favours wound matrix degradation, thus, amplifying a pre-existing granulation tissue productive cells' invasiveness and recruitment deficit. Tumour necrosis factor perpetuates homing of inflammatory cells, triggers pro-apoptotic genes and impairs reepithelialisation. Advanced glycation end-products act in concert with inflammatory mediators and commit fibroblasts and vascular cells to apoptosis, contributing to granulation tissue demise. Therapeutic approaches aimed to downregulate hyperinflammation and/or attenuate glucolipotoxicity may assist in diabetic wound healing by dismantling downstream effectors. These medical interventions are demanded to reduce amputations in an expanding diabetic population.
Jorge Berlanga Acosta; Diana Garcia del Barco; Danay Cibrian Vera; William Savigne; Pedro Lopez-Saura; Gerardo Guillen Nieto; Gregory S Schultz
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Publication Detail:
Type:  Journal Article; Review    
Journal Detail:
Title:  International wound journal     Volume:  5     ISSN:  1742-481X     ISO Abbreviation:  -     Publication Date:  2008 Oct 
Date Detail:
Created Date:  2008-11-13     Completed Date:  2009-02-04     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  101230907     Medline TA:  Int Wound J     Country:  England    
Other Details:
Languages:  eng     Pagination:  530-9     Citation Subset:  IM    
Biomedical Research Direction, Pharmaceutical Division, Center for Genetic Engineering and Biotechnology, Avenida 31 e/158 y 190, Playa, PO Box 6162, Havana 10600, Cuba.
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MeSH Terms
Apoptosis / immunology
Apoptosis Regulatory Proteins / immunology
Diabetic Foot / immunology*,  prevention & control
Down-Regulation / drug effects,  immunology
Fibroblasts / immunology
Glycosylation End Products, Advanced / antagonists & inhibitors,  immunology*
Granulation Tissue / immunology
Matrix Metalloproteinases / immunology*
Tumor Necrosis Factors / antagonists & inhibitors,  immunology*
Wound Healing / drug effects,  immunology*
Reg. No./Substance:
0/Apoptosis Regulatory Proteins; 0/Glycosylation End Products, Advanced; 0/Tumor Necrosis Factors; EC 3.4.24.-/Matrix Metalloproteinases

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

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