Diabetic nephropathy: protective factors and a new therapeutic paradigm
Abstract Diabetic nephropathy (DN) is the most common cause of chronic kidney disease (CKD) and its number has been increasing. CKD is a worldwide threat to health but the precise mechanism of this problem is not fully appreciated. It is believed that hyperglycemia is one of the most important metab...
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Veröffentlicht in: | Journal of diabetes and its complications 2013-09, Vol.27 (5), p.526-530 |
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description | Abstract Diabetic nephropathy (DN) is the most common cause of chronic kidney disease (CKD) and its number has been increasing. CKD is a worldwide threat to health but the precise mechanism of this problem is not fully appreciated. It is believed that hyperglycemia is one of the most important metabolic factors in the development of DN. Multiple molecular mechanisms have been proposed to mediate hyperglycemia’s adverse effects on kidney. To identify targets for therapeutic intervention, most studies have focused on understanding how abnormal levels of such metabolities cause DN. However, there have been few reports regarding endogenous renal protective factors. Thus, recognition of the importance of this could be providing a new perspective for understanding the development of DN and a new therapeutic paradigm to combat DN. |
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CKD is a worldwide threat to health but the precise mechanism of this problem is not fully appreciated. It is believed that hyperglycemia is one of the most important metabolic factors in the development of DN. Multiple molecular mechanisms have been proposed to mediate hyperglycemia’s adverse effects on kidney. To identify targets for therapeutic intervention, most studies have focused on understanding how abnormal levels of such metabolities cause DN. However, there have been few reports regarding endogenous renal protective factors. Thus, recognition of the importance of this could be providing a new perspective for understanding the development of DN and a new therapeutic paradigm to combat DN.</description><identifier>ISSN: 1056-8727</identifier><identifier>EISSN: 1873-460X</identifier><identifier>DOI: 10.1016/j.jdiacomp.2013.03.003</identifier><identifier>PMID: 23619194</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Angiopoietins ; Animals ; Cytoprotection - drug effects ; Cytoprotection - physiology ; Diabetes ; Diabetic Nephropathies - prevention & control ; Diabetic Nephropathies - therapy ; Diabetic nephropathy (DN) ; Dipeptidyl peptidase-4 (DPP-4) inhibitors ; Dipeptidyl-Peptidase IV Inhibitors - pharmacology ; Dipeptidyl-Peptidase IV Inhibitors - therapeutic use ; Endocrinology & Metabolism ; Endostatin ; Glucagon like peptide-1 (GLP-1) ; Glucagon-Like Peptide 1 - physiology ; Heme Oxygenase-1 - physiology ; Humans ; Hyperglycemia ; Hypoglycemic Agents - therapeutic use ; Insulin ; Insulin - pharmacology ; Insulin - therapeutic use ; Insulin receptor substrate 1 (IRS1) ; Insulin resistance ; Kidney - drug effects ; Kidney - physiology ; Kinases ; Muscular system ; Protein kinase C (PKC) ; Src homology-2 domain containing phosphatase-1 (SHP-1) ; Tumstatin ; Vascular endothelial growth factor (VEGF) ; Vascular Endothelial Growth Factor A - physiology</subject><ispartof>Journal of diabetes and its complications, 2013-09, Vol.27 (5), p.526-530</ispartof><rights>Elsevier Inc.</rights><rights>2013 Elsevier Inc.</rights><rights>Copyright © 2013 Elsevier Inc. All rights reserved.</rights><rights>Copyright Elsevier Limited Sep 2013</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c583t-59582a3702db231720f24a5e7e6a03588dce57d5b973d6a816a2ac73f2cf3e733</citedby><cites>FETCH-LOGICAL-c583t-59582a3702db231720f24a5e7e6a03588dce57d5b973d6a816a2ac73f2cf3e733</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.proquest.com/docview/1430634975?pq-origsite=primo$$EHTML$$P50$$Gproquest$$H</linktohtml><link.rule.ids>314,777,781,3537,27905,27906,45976,64364,64366,64368,72218</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23619194$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Mima, Akira</creatorcontrib><title>Diabetic nephropathy: protective factors and a new therapeutic paradigm</title><title>Journal of diabetes and its complications</title><addtitle>J Diabetes Complications</addtitle><description>Abstract Diabetic nephropathy (DN) is the most common cause of chronic kidney disease (CKD) and its number has been increasing. CKD is a worldwide threat to health but the precise mechanism of this problem is not fully appreciated. It is believed that hyperglycemia is one of the most important metabolic factors in the development of DN. Multiple molecular mechanisms have been proposed to mediate hyperglycemia’s adverse effects on kidney. To identify targets for therapeutic intervention, most studies have focused on understanding how abnormal levels of such metabolities cause DN. However, there have been few reports regarding endogenous renal protective factors. Thus, recognition of the importance of this could be providing a new perspective for understanding the development of DN and a new therapeutic paradigm to combat DN.</description><subject>Angiopoietins</subject><subject>Animals</subject><subject>Cytoprotection - drug effects</subject><subject>Cytoprotection - physiology</subject><subject>Diabetes</subject><subject>Diabetic Nephropathies - prevention & control</subject><subject>Diabetic Nephropathies - therapy</subject><subject>Diabetic nephropathy (DN)</subject><subject>Dipeptidyl peptidase-4 (DPP-4) inhibitors</subject><subject>Dipeptidyl-Peptidase IV Inhibitors - pharmacology</subject><subject>Dipeptidyl-Peptidase IV Inhibitors - therapeutic use</subject><subject>Endocrinology & Metabolism</subject><subject>Endostatin</subject><subject>Glucagon like peptide-1 (GLP-1)</subject><subject>Glucagon-Like Peptide 1 - physiology</subject><subject>Heme Oxygenase-1 - physiology</subject><subject>Humans</subject><subject>Hyperglycemia</subject><subject>Hypoglycemic Agents - therapeutic use</subject><subject>Insulin</subject><subject>Insulin - pharmacology</subject><subject>Insulin - therapeutic use</subject><subject>Insulin receptor substrate 1 (IRS1)</subject><subject>Insulin resistance</subject><subject>Kidney - drug effects</subject><subject>Kidney - physiology</subject><subject>Kinases</subject><subject>Muscular system</subject><subject>Protein kinase C (PKC)</subject><subject>Src homology-2 domain containing phosphatase-1 (SHP-1)</subject><subject>Tumstatin</subject><subject>Vascular endothelial growth factor (VEGF)</subject><subject>Vascular Endothelial Growth Factor A - physiology</subject><issn>1056-8727</issn><issn>1873-460X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNqNkk1v1DAQhiMEoqXwF6pIXLhkGdvxRzggUIGCVIkDIHGzZu0J67D5wE6K9t_jaFuQeinSSPbhmdfz-p2iOGewYcDUy27T-YBu7KcNByY2kAvEg-KUGS2qWsH3h_kOUlVGc31SPEmpAwAlJXtcnHChWMOa-rS4fBdwS3Nw5UDTLo4TzrvDq3KK40xuDtdUtujmMaYSB19ipn6X844iTrSsXRNG9OFH_7R41OI-0bOb86z49uH914uP1dXny08Xb68qJ42YK9lIw1Fo4H7LBdMcWl6jJE0KQUhjvCOpvdw2WniFhink6LRouWsFaSHOihdH3Tzhr4XSbPuQHO33ONC4JMsM1w2A4fX9aK0UNLyW8j9QwRTnqmYZfX4H7cYlDtnzSoESdaNXQXWkXBxTitTaKYYe48EysGuAtrO3Ado1QAu5YPV3fiO_bHvyf9tuE8vAmyNA-ZevA0WbXKDBkQ8xJ2b9GO5_4_UdCbcPQ3C4_0kHSv_82MQt2C_rGq1bxETeIGmk-APzEMII</recordid><startdate>20130901</startdate><enddate>20130901</enddate><creator>Mima, Akira</creator><general>Elsevier Inc</general><general>Elsevier Limited</general><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>7RV</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AN0</scope><scope>ASE</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FPQ</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>K6X</scope><scope>K9-</scope><scope>K9.</scope><scope>KB0</scope><scope>M0R</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>MBDVC</scope><scope>NAPCQ</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope><scope>7T5</scope><scope>H94</scope></search><sort><creationdate>20130901</creationdate><title>Diabetic nephropathy: protective factors and a new therapeutic paradigm</title><author>Mima, Akira</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c583t-59582a3702db231720f24a5e7e6a03588dce57d5b973d6a816a2ac73f2cf3e733</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>Angiopoietins</topic><topic>Animals</topic><topic>Cytoprotection - drug effects</topic><topic>Cytoprotection - physiology</topic><topic>Diabetes</topic><topic>Diabetic Nephropathies - prevention & control</topic><topic>Diabetic Nephropathies - therapy</topic><topic>Diabetic nephropathy (DN)</topic><topic>Dipeptidyl peptidase-4 (DPP-4) inhibitors</topic><topic>Dipeptidyl-Peptidase IV Inhibitors - pharmacology</topic><topic>Dipeptidyl-Peptidase IV Inhibitors - therapeutic use</topic><topic>Endocrinology & Metabolism</topic><topic>Endostatin</topic><topic>Glucagon like peptide-1 (GLP-1)</topic><topic>Glucagon-Like Peptide 1 - physiology</topic><topic>Heme Oxygenase-1 - physiology</topic><topic>Humans</topic><topic>Hyperglycemia</topic><topic>Hypoglycemic Agents - therapeutic use</topic><topic>Insulin</topic><topic>Insulin - pharmacology</topic><topic>Insulin - therapeutic use</topic><topic>Insulin receptor substrate 1 (IRS1)</topic><topic>Insulin resistance</topic><topic>Kidney - drug effects</topic><topic>Kidney - physiology</topic><topic>Kinases</topic><topic>Muscular system</topic><topic>Protein kinase C (PKC)</topic><topic>Src homology-2 domain containing phosphatase-1 (SHP-1)</topic><topic>Tumstatin</topic><topic>Vascular endothelial growth factor (VEGF)</topic><topic>Vascular Endothelial Growth Factor A - 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Academic</collection><collection>Immunology Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><jtitle>Journal of diabetes and its complications</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Mima, Akira</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Diabetic nephropathy: protective factors and a new therapeutic paradigm</atitle><jtitle>Journal of diabetes and its complications</jtitle><addtitle>J Diabetes Complications</addtitle><date>2013-09-01</date><risdate>2013</risdate><volume>27</volume><issue>5</issue><spage>526</spage><epage>530</epage><pages>526-530</pages><issn>1056-8727</issn><eissn>1873-460X</eissn><abstract>Abstract Diabetic nephropathy (DN) is the most common cause of chronic kidney disease (CKD) and its number has been increasing. CKD is a worldwide threat to health but the precise mechanism of this problem is not fully appreciated. It is believed that hyperglycemia is one of the most important metabolic factors in the development of DN. Multiple molecular mechanisms have been proposed to mediate hyperglycemia’s adverse effects on kidney. To identify targets for therapeutic intervention, most studies have focused on understanding how abnormal levels of such metabolities cause DN. However, there have been few reports regarding endogenous renal protective factors. Thus, recognition of the importance of this could be providing a new perspective for understanding the development of DN and a new therapeutic paradigm to combat DN.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>23619194</pmid><doi>10.1016/j.jdiacomp.2013.03.003</doi><tpages>5</tpages></addata></record> |
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subjects | Angiopoietins Animals Cytoprotection - drug effects Cytoprotection - physiology Diabetes Diabetic Nephropathies - prevention & control Diabetic Nephropathies - therapy Diabetic nephropathy (DN) Dipeptidyl peptidase-4 (DPP-4) inhibitors Dipeptidyl-Peptidase IV Inhibitors - pharmacology Dipeptidyl-Peptidase IV Inhibitors - therapeutic use Endocrinology & Metabolism Endostatin Glucagon like peptide-1 (GLP-1) Glucagon-Like Peptide 1 - physiology Heme Oxygenase-1 - physiology Humans Hyperglycemia Hypoglycemic Agents - therapeutic use Insulin Insulin - pharmacology Insulin - therapeutic use Insulin receptor substrate 1 (IRS1) Insulin resistance Kidney - drug effects Kidney - physiology Kinases Muscular system Protein kinase C (PKC) Src homology-2 domain containing phosphatase-1 (SHP-1) Tumstatin Vascular endothelial growth factor (VEGF) Vascular Endothelial Growth Factor A - physiology |
title | Diabetic nephropathy: protective factors and a new therapeutic paradigm |
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