Putative pathophysiological role of growth factors and cytokines in experimental diabetic kidney disease
The development of diabetic nephropathy in patients with Type I (insulin-dependent) and Type II (non-insulin-dependent) diabetes mellitus is still a huge clinical problem associated with increased morbidity and mortality. The mechanisms underlying the development of diabetic kidney disease are extre...
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| description | The development of diabetic nephropathy in patients with Type I (insulin-dependent) and Type II (non-insulin-dependent) diabetes mellitus is still a huge clinical problem associated with increased morbidity and mortality. The mechanisms underlying the development of diabetic kidney disease are extremely complex and yet not completely understood. Among many potential pathogenic mechanisms responsible for the development of diabetic kidney disease, various growth factors have been suggested to be important players. In particular, growth hormone (GH)/insulin-like growth factors (IGFs), transforming growth factor beta (TGF-beta), vascular endothelial growth factor (VEGF) and epidermal growth factor (EGF) have measurable effects on the development of experimental diabetic kidney disease through complex intra-renal systems. Recent findings that these growth factors might initiate the early diabetic renal changes have provided insight into processes that might be relevant for future development of new drugs useful in the treatment of diabetic kidney disease. As will appear from the present review, enhanced understanding of the cellular mechanisms responsible for the development of diabetic kidney disease has already allowed the design of specific antagonists of pathophysiologically increased growth factors. Recent studies have shown that treating experimental diabetic models with such antagonists is followed by renoprotection. |
| doi_str_mv | 10.1007/s001250051515 |
| format | Article |
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The mechanisms underlying the development of diabetic kidney disease are extremely complex and yet not completely understood. Among many potential pathogenic mechanisms responsible for the development of diabetic kidney disease, various growth factors have been suggested to be important players. In particular, growth hormone (GH)/insulin-like growth factors (IGFs), transforming growth factor beta (TGF-beta), vascular endothelial growth factor (VEGF) and epidermal growth factor (EGF) have measurable effects on the development of experimental diabetic kidney disease through complex intra-renal systems. Recent findings that these growth factors might initiate the early diabetic renal changes have provided insight into processes that might be relevant for future development of new drugs useful in the treatment of diabetic kidney disease. 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Apud cells (diseases) ; Endocrinology ; Endocrinopathies ; Endothelial Growth Factors - physiology ; Enzymes ; Epidermal growth factor ; Epidermal Growth Factor - physiology ; Extracellular matrix ; Growth Hormone - physiology ; Growth hormones ; Growth Substances - physiology ; Humans ; Insulin ; Insulin-like growth factors ; Kidney diseases ; Kinases ; Lymphokines - physiology ; Medical research ; Medical sciences ; Metabolism ; Pathogenesis ; Proteins ; Somatomedins - physiology ; Transforming Growth Factor beta - physiology ; Vascular endothelial growth factor ; Vascular Endothelial Growth Factor A ; Vascular Endothelial Growth Factors</subject><ispartof>Diabetologia, 2000-10, Vol.43 (10), p.1205-1223</ispartof><rights>2001 INIST-CNRS</rights><rights>Springer-Verlag Berlin Heidelberg 2000</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c449t-5c0c8633dcace6d24aaef420516e4b21e028874fb683d3926f75d65621d82a843</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>315,782,786,27933,27934</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=827597$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/11079738$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>FLYVBJERG, A</creatorcontrib><title>Putative pathophysiological role of growth factors and cytokines in experimental diabetic kidney disease</title><title>Diabetologia</title><addtitle>Diabetologia</addtitle><description>The development of diabetic nephropathy in patients with Type I (insulin-dependent) and Type II (non-insulin-dependent) diabetes mellitus is still a huge clinical problem associated with increased morbidity and mortality. The mechanisms underlying the development of diabetic kidney disease are extremely complex and yet not completely understood. Among many potential pathogenic mechanisms responsible for the development of diabetic kidney disease, various growth factors have been suggested to be important players. In particular, growth hormone (GH)/insulin-like growth factors (IGFs), transforming growth factor beta (TGF-beta), vascular endothelial growth factor (VEGF) and epidermal growth factor (EGF) have measurable effects on the development of experimental diabetic kidney disease through complex intra-renal systems. Recent findings that these growth factors might initiate the early diabetic renal changes have provided insight into processes that might be relevant for future development of new drugs useful in the treatment of diabetic kidney disease. As will appear from the present review, enhanced understanding of the cellular mechanisms responsible for the development of diabetic kidney disease has already allowed the design of specific antagonists of pathophysiologically increased growth factors. Recent studies have shown that treating experimental diabetic models with such antagonists is followed by renoprotection.</description><subject>Animals</subject><subject>Associated diseases and complications</subject><subject>Biological and medical sciences</subject><subject>Cytokines</subject><subject>Cytokines - physiology</subject><subject>Diabetes</subject><subject>Diabetes. Impaired glucose tolerance</subject><subject>Diabetic Nephropathies - physiopathology</subject><subject>Diabetic nephropathy</subject><subject>Endocrine pancreas. Apud cells (diseases)</subject><subject>Endocrinology</subject><subject>Endocrinopathies</subject><subject>Endothelial Growth Factors - physiology</subject><subject>Enzymes</subject><subject>Epidermal growth factor</subject><subject>Epidermal Growth Factor - physiology</subject><subject>Extracellular matrix</subject><subject>Growth Hormone - physiology</subject><subject>Growth hormones</subject><subject>Growth Substances - physiology</subject><subject>Humans</subject><subject>Insulin</subject><subject>Insulin-like growth factors</subject><subject>Kidney diseases</subject><subject>Kinases</subject><subject>Lymphokines - physiology</subject><subject>Medical research</subject><subject>Medical sciences</subject><subject>Metabolism</subject><subject>Pathogenesis</subject><subject>Proteins</subject><subject>Somatomedins - physiology</subject><subject>Transforming Growth Factor beta - physiology</subject><subject>Vascular endothelial growth factor</subject><subject>Vascular Endothelial Growth Factor A</subject><subject>Vascular Endothelial Growth Factors</subject><issn>0012-186X</issn><issn>1432-0428</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2000</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNpd0M1LHDEYBvAgLbpVj15LaKG3qfmaJHsUqVoQ2kMFb0MmecfN7uxkTDK189834mCx5BBCfnnI-yB0RslXSog6T4RQVhNS07IO0IoKzioimH6HVs9XFdXy_gh9SGlLCOG1kIfoiFKi1orrFdr8nLLJ_jfg0eRNGDdz8qEPD96aHsfQAw4dfojhKW9wZ2wOMWEzOGznHHZ-gIT9gOHPCNHvYcjlkfOmhewt3nk3wFzOCUyCE_S-M32C02U_RndX335d3lS3P66_X17cVlaIda5qS6yWnDtrLEjHhDHQCVbGkyBaRoEwrZXoWqm542smO1U7WUtGnWZGC36MvrzkjjE8TpBys_fJQt-bAcKUGsUEZYrIAj_9B7dhikP5W8MoL0miVgVVL8jGkFKErhnLoCbODSXNc__Nm_6L_7iETu0e3D-9FF7A5wWYVCruohmsT69OM1UX9xczJ40_</recordid><startdate>20001001</startdate><enddate>20001001</enddate><creator>FLYVBJERG, A</creator><general>Springer</general><general>Springer Nature B.V</general><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>3V.</scope><scope>7T5</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>H94</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope></search><sort><creationdate>20001001</creationdate><title>Putative pathophysiological role of growth factors and cytokines in experimental diabetic kidney disease</title><author>FLYVBJERG, A</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c449t-5c0c8633dcace6d24aaef420516e4b21e028874fb683d3926f75d65621d82a843</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2000</creationdate><topic>Animals</topic><topic>Associated diseases and complications</topic><topic>Biological and medical sciences</topic><topic>Cytokines</topic><topic>Cytokines - physiology</topic><topic>Diabetes</topic><topic>Diabetes. Impaired glucose tolerance</topic><topic>Diabetic Nephropathies - physiopathology</topic><topic>Diabetic nephropathy</topic><topic>Endocrine pancreas. Apud cells (diseases)</topic><topic>Endocrinology</topic><topic>Endocrinopathies</topic><topic>Endothelial Growth Factors - physiology</topic><topic>Enzymes</topic><topic>Epidermal growth factor</topic><topic>Epidermal Growth Factor - physiology</topic><topic>Extracellular matrix</topic><topic>Growth Hormone - physiology</topic><topic>Growth hormones</topic><topic>Growth Substances - physiology</topic><topic>Humans</topic><topic>Insulin</topic><topic>Insulin-like growth factors</topic><topic>Kidney diseases</topic><topic>Kinases</topic><topic>Lymphokines - physiology</topic><topic>Medical research</topic><topic>Medical sciences</topic><topic>Metabolism</topic><topic>Pathogenesis</topic><topic>Proteins</topic><topic>Somatomedins - physiology</topic><topic>Transforming Growth Factor beta - physiology</topic><topic>Vascular endothelial growth factor</topic><topic>Vascular Endothelial Growth Factor A</topic><topic>Vascular Endothelial Growth Factors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>FLYVBJERG, A</creatorcontrib><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>ProQuest Central (Corporate)</collection><collection>Immunology Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><jtitle>Diabetologia</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>FLYVBJERG, A</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Putative pathophysiological role of growth factors and cytokines in experimental diabetic kidney disease</atitle><jtitle>Diabetologia</jtitle><addtitle>Diabetologia</addtitle><date>2000-10-01</date><risdate>2000</risdate><volume>43</volume><issue>10</issue><spage>1205</spage><epage>1223</epage><pages>1205-1223</pages><issn>0012-186X</issn><eissn>1432-0428</eissn><abstract>The development of diabetic nephropathy in patients with Type I (insulin-dependent) and Type II (non-insulin-dependent) diabetes mellitus is still a huge clinical problem associated with increased morbidity and mortality. The mechanisms underlying the development of diabetic kidney disease are extremely complex and yet not completely understood. Among many potential pathogenic mechanisms responsible for the development of diabetic kidney disease, various growth factors have been suggested to be important players. In particular, growth hormone (GH)/insulin-like growth factors (IGFs), transforming growth factor beta (TGF-beta), vascular endothelial growth factor (VEGF) and epidermal growth factor (EGF) have measurable effects on the development of experimental diabetic kidney disease through complex intra-renal systems. Recent findings that these growth factors might initiate the early diabetic renal changes have provided insight into processes that might be relevant for future development of new drugs useful in the treatment of diabetic kidney disease. As will appear from the present review, enhanced understanding of the cellular mechanisms responsible for the development of diabetic kidney disease has already allowed the design of specific antagonists of pathophysiologically increased growth factors. Recent studies have shown that treating experimental diabetic models with such antagonists is followed by renoprotection.</abstract><cop>Berlin</cop><pub>Springer</pub><pmid>11079738</pmid><doi>10.1007/s001250051515</doi><tpages>19</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Associated diseases and complications Biological and medical sciences Cytokines Cytokines - physiology Diabetes Diabetes. Impaired glucose tolerance Diabetic Nephropathies - physiopathology Diabetic nephropathy Endocrine pancreas. Apud cells (diseases) Endocrinology Endocrinopathies Endothelial Growth Factors - physiology Enzymes Epidermal growth factor Epidermal Growth Factor - physiology Extracellular matrix Growth Hormone - physiology Growth hormones Growth Substances - physiology Humans Insulin Insulin-like growth factors Kidney diseases Kinases Lymphokines - physiology Medical research Medical sciences Metabolism Pathogenesis Proteins Somatomedins - physiology Transforming Growth Factor beta - physiology Vascular endothelial growth factor Vascular Endothelial Growth Factor A Vascular Endothelial Growth Factors |
| title | Putative pathophysiological role of growth factors and cytokines in experimental diabetic kidney disease |
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