The molecular biology of chronic wounds and delayed healing in diabetes
Wound healing is a complicated and integrated process. Although there is some tolerance in terms of redundancy and interrelated control mechanisms, pushing beyond such limits may contribute to delayed wound healing, and in extreme cases lead to chronic wounds/ulcers and thus potentially to lower ext...
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Veröffentlicht in: | Diabetic medicine 2006-06, Vol.23 (6), p.594-608 |
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description | Wound healing is a complicated and integrated process. Although there is some tolerance in terms of redundancy and interrelated control mechanisms, pushing beyond such limits may contribute to delayed wound healing, and in extreme cases lead to chronic wounds/ulcers and thus potentially to lower extremity amputation. Diabetes is associated with such disruption in wound healing. Research in humans and in animal models has identified a large number of changes associated with diabetes at the molecular level in delayed wound healing and to a lesser extent in chronic diabetic ulcers. Better overall understanding of these changes and how they are interrelated would allow for specifically targeted treatment, thus ensuring improved quality of life for patients and providing savings to the high costs that are associated with all aspects of chronic diabetic ulcers. This review examines the work done at the molecular level on chronic diabetic ulcers, as well as considering changes seen in diabetes in general, both in humans and animal models, that may in turn contribute to ulcer formation. |
doi_str_mv | 10.1111/j.1464-5491.2006.01773.x |
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Although there is some tolerance in terms of redundancy and interrelated control mechanisms, pushing beyond such limits may contribute to delayed wound healing, and in extreme cases lead to chronic wounds/ulcers and thus potentially to lower extremity amputation. Diabetes is associated with such disruption in wound healing. Research in humans and in animal models has identified a large number of changes associated with diabetes at the molecular level in delayed wound healing and to a lesser extent in chronic diabetic ulcers. Better overall understanding of these changes and how they are interrelated would allow for specifically targeted treatment, thus ensuring improved quality of life for patients and providing savings to the high costs that are associated with all aspects of chronic diabetic ulcers. This review examines the work done at the molecular level on chronic diabetic ulcers, as well as considering changes seen in diabetes in general, both in humans and animal models, that may in turn contribute to ulcer formation.</description><identifier>ISSN: 0742-3071</identifier><identifier>EISSN: 1464-5491</identifier><identifier>DOI: 10.1111/j.1464-5491.2006.01773.x</identifier><identifier>PMID: 16759300</identifier><identifier>CODEN: DIMEEV</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Publishing Ltd</publisher><subject>Animals ; Biological and medical sciences ; chronic wounds ; Cytokines - genetics ; Cytokines - metabolism ; Diabetes Complications - metabolism ; Diabetes Complications - pathology ; Diabetes Mellitus, Experimental - metabolism ; Diabetes Mellitus, Experimental - pathology ; Diabetes. Impaired glucose tolerance ; Endocrine pancreas. Apud cells (diseases) ; Endocrinopathies ; Etiopathogenesis. Screening. Investigations. Target tissue resistance ; Extracellular Matrix - metabolism ; Extracellular Matrix - pathology ; Glucose - metabolism ; growth factors ; Humans ; Intercellular Signaling Peptides and Proteins - genetics ; Intercellular Signaling Peptides and Proteins - physiology ; matrix metalloproteinases ; Medical sciences ; nitric oxide ; Nitric Oxide - metabolism ; Oxidation-Reduction ; Skin - blood supply ; Skin - metabolism ; Skin - pathology ; wound healing ; Wound Healing - physiology</subject><ispartof>Diabetic medicine, 2006-06, Vol.23 (6), p.594-608</ispartof><rights>2006 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5013-2252729b1108fa7b58e544e84bb813e80550f1108e6005e168acd88755f81d973</citedby><cites>FETCH-LOGICAL-c5013-2252729b1108fa7b58e544e84bb813e80550f1108e6005e168acd88755f81d973</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1111%2Fj.1464-5491.2006.01773.x$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Fj.1464-5491.2006.01773.x$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,780,784,1417,27924,27925,45574,45575</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=17828873$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/16759300$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Blakytny, R.</creatorcontrib><creatorcontrib>Jude, E.</creatorcontrib><title>The molecular biology of chronic wounds and delayed healing in diabetes</title><title>Diabetic medicine</title><addtitle>Diabet Med</addtitle><description>Wound healing is a complicated and integrated process. Although there is some tolerance in terms of redundancy and interrelated control mechanisms, pushing beyond such limits may contribute to delayed wound healing, and in extreme cases lead to chronic wounds/ulcers and thus potentially to lower extremity amputation. Diabetes is associated with such disruption in wound healing. Research in humans and in animal models has identified a large number of changes associated with diabetes at the molecular level in delayed wound healing and to a lesser extent in chronic diabetic ulcers. Better overall understanding of these changes and how they are interrelated would allow for specifically targeted treatment, thus ensuring improved quality of life for patients and providing savings to the high costs that are associated with all aspects of chronic diabetic ulcers. This review examines the work done at the molecular level on chronic diabetic ulcers, as well as considering changes seen in diabetes in general, both in humans and animal models, that may in turn contribute to ulcer formation.</description><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>chronic wounds</subject><subject>Cytokines - genetics</subject><subject>Cytokines - metabolism</subject><subject>Diabetes Complications - metabolism</subject><subject>Diabetes Complications - pathology</subject><subject>Diabetes Mellitus, Experimental - metabolism</subject><subject>Diabetes Mellitus, Experimental - pathology</subject><subject>Diabetes. Impaired glucose tolerance</subject><subject>Endocrine pancreas. Apud cells (diseases)</subject><subject>Endocrinopathies</subject><subject>Etiopathogenesis. Screening. Investigations. Target tissue resistance</subject><subject>Extracellular Matrix - metabolism</subject><subject>Extracellular Matrix - pathology</subject><subject>Glucose - metabolism</subject><subject>growth factors</subject><subject>Humans</subject><subject>Intercellular Signaling Peptides and Proteins - genetics</subject><subject>Intercellular Signaling Peptides and Proteins - physiology</subject><subject>matrix metalloproteinases</subject><subject>Medical sciences</subject><subject>nitric oxide</subject><subject>Nitric Oxide - metabolism</subject><subject>Oxidation-Reduction</subject><subject>Skin - blood supply</subject><subject>Skin - metabolism</subject><subject>Skin - pathology</subject><subject>wound healing</subject><subject>Wound Healing - physiology</subject><issn>0742-3071</issn><issn>1464-5491</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2006</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkE1v1DAQhi0EokvhLyBf4JbU33YOHFBbtvRTSIs4Wo4z6Xrxxm28UXf_PUl31V7xZSzN886MHoQwJSUd38mqpEKJQoqKlowQVRKqNS-3b9DspfEWzYgWrOBE0yP0IecVIZRVvHqPjqjSsuKEzNB8sQS8ThH8EF2P65Biut_h1GK_7FMXPH5KQ9dk7LoGNxDdDhq8BBdDd49Dh5vgathA_ojetS5m-HSox-j3j_PF6UVxfTf_efr9uvCSUF4wJplmVU0pMa3TtTQghQAj6tpQDoZISdqpCYoQCVQZ5xtjtJStoU2l-TH6up_70KfHAfLGrkP2EKPrIA3ZKkOEYFSNoNmDvk8599Dahz6sXb-zlNhJol3ZyZWdXNlJon2WaLdj9PNhx1CvoXkNHqyNwJcD4LJ3se1d50N-5bRh48185L7tuacQYfffB9izm_PpN-aLfT7kDWxf8q7_a5XmWto_t3P76_bqUi3OKnvB_wETCJo5</recordid><startdate>200606</startdate><enddate>200606</enddate><creator>Blakytny, R.</creator><creator>Jude, E.</creator><general>Blackwell Publishing Ltd</general><general>Blackwell</general><scope>BSCLL</scope><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>200606</creationdate><title>The molecular biology of chronic wounds and delayed healing in diabetes</title><author>Blakytny, R. ; Jude, E.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5013-2252729b1108fa7b58e544e84bb813e80550f1108e6005e168acd88755f81d973</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2006</creationdate><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>chronic wounds</topic><topic>Cytokines - genetics</topic><topic>Cytokines - metabolism</topic><topic>Diabetes Complications - metabolism</topic><topic>Diabetes Complications - pathology</topic><topic>Diabetes Mellitus, Experimental - metabolism</topic><topic>Diabetes Mellitus, Experimental - pathology</topic><topic>Diabetes. Impaired glucose tolerance</topic><topic>Endocrine pancreas. Apud cells (diseases)</topic><topic>Endocrinopathies</topic><topic>Etiopathogenesis. Screening. Investigations. Target tissue resistance</topic><topic>Extracellular Matrix - metabolism</topic><topic>Extracellular Matrix - pathology</topic><topic>Glucose - metabolism</topic><topic>growth factors</topic><topic>Humans</topic><topic>Intercellular Signaling Peptides and Proteins - genetics</topic><topic>Intercellular Signaling Peptides and Proteins - physiology</topic><topic>matrix metalloproteinases</topic><topic>Medical sciences</topic><topic>nitric oxide</topic><topic>Nitric Oxide - metabolism</topic><topic>Oxidation-Reduction</topic><topic>Skin - blood supply</topic><topic>Skin - metabolism</topic><topic>Skin - pathology</topic><topic>wound healing</topic><topic>Wound Healing - physiology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Blakytny, R.</creatorcontrib><creatorcontrib>Jude, E.</creatorcontrib><collection>Istex</collection><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Diabetic medicine</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Blakytny, R.</au><au>Jude, E.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The molecular biology of chronic wounds and delayed healing in diabetes</atitle><jtitle>Diabetic medicine</jtitle><addtitle>Diabet Med</addtitle><date>2006-06</date><risdate>2006</risdate><volume>23</volume><issue>6</issue><spage>594</spage><epage>608</epage><pages>594-608</pages><issn>0742-3071</issn><eissn>1464-5491</eissn><coden>DIMEEV</coden><abstract>Wound healing is a complicated and integrated process. Although there is some tolerance in terms of redundancy and interrelated control mechanisms, pushing beyond such limits may contribute to delayed wound healing, and in extreme cases lead to chronic wounds/ulcers and thus potentially to lower extremity amputation. Diabetes is associated with such disruption in wound healing. Research in humans and in animal models has identified a large number of changes associated with diabetes at the molecular level in delayed wound healing and to a lesser extent in chronic diabetic ulcers. Better overall understanding of these changes and how they are interrelated would allow for specifically targeted treatment, thus ensuring improved quality of life for patients and providing savings to the high costs that are associated with all aspects of chronic diabetic ulcers. This review examines the work done at the molecular level on chronic diabetic ulcers, as well as considering changes seen in diabetes in general, both in humans and animal models, that may in turn contribute to ulcer formation.</abstract><cop>Oxford, UK</cop><pub>Blackwell Publishing Ltd</pub><pmid>16759300</pmid><doi>10.1111/j.1464-5491.2006.01773.x</doi><tpages>15</tpages></addata></record> |
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subjects | Animals Biological and medical sciences chronic wounds Cytokines - genetics Cytokines - metabolism Diabetes Complications - metabolism Diabetes Complications - pathology Diabetes Mellitus, Experimental - metabolism Diabetes Mellitus, Experimental - pathology Diabetes. Impaired glucose tolerance Endocrine pancreas. Apud cells (diseases) Endocrinopathies Etiopathogenesis. Screening. Investigations. Target tissue resistance Extracellular Matrix - metabolism Extracellular Matrix - pathology Glucose - metabolism growth factors Humans Intercellular Signaling Peptides and Proteins - genetics Intercellular Signaling Peptides and Proteins - physiology matrix metalloproteinases Medical sciences nitric oxide Nitric Oxide - metabolism Oxidation-Reduction Skin - blood supply Skin - metabolism Skin - pathology wound healing Wound Healing - physiology |
title | The molecular biology of chronic wounds and delayed healing in diabetes |
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