<?xml version="1.0" encoding="UTF-8"?>
<collection xmlns="http://www.loc.gov/MARC21/slim">
 <record>
  <leader>     caa a22        4500</leader>
  <controlfield tag="001">475772229</controlfield>
  <controlfield tag="003">CHVBK</controlfield>
  <controlfield tag="005">20180406123620.0</controlfield>
  <controlfield tag="007">cr unu---uuuuu</controlfield>
  <controlfield tag="008">170329e20001001xx      s     000 0 eng  </controlfield>
  <datafield tag="024" ind1="7" ind2="0">
   <subfield code="a">10.1007/s001250051515</subfield>
   <subfield code="2">doi</subfield>
  </datafield>
  <datafield tag="035" ind1=" " ind2=" ">
   <subfield code="a">(NATIONALLICENCE)springer-10.1007/s001250051515</subfield>
  </datafield>
  <datafield tag="100" ind1="1" ind2=" ">
   <subfield code="a">Flyvbjerg</subfield>
   <subfield code="D">A.</subfield>
   <subfield code="u">Medical Research Laboratory M (Diabetes and Endocrinology) and Medical Department M (Diabetes and Endocrinology), Institute of Experimental Clinical Research, University of Aarhus, Aarhus Community Hospital, Aarhus, Denmark, DK</subfield>
   <subfield code="4">aut</subfield>
  </datafield>
  <datafield tag="245" ind1="1" ind2="0">
   <subfield code="a">Putative pathophysiological role of growth factors and cytokines in experimental diabetic kidney disease</subfield>
   <subfield code="h">[Elektronische Daten]</subfield>
   <subfield code="c">[A. Flyvbjerg]</subfield>
  </datafield>
  <datafield tag="520" ind1="3" ind2=" ">
   <subfield code="a">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 β (TGF-β), 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. [Diabetologia (2000) 43: 1205-1223]</subfield>
  </datafield>
  <datafield tag="540" ind1=" " ind2=" ">
   <subfield code="a">Springer-Verlag Berlin Heidelberg, 2000</subfield>
  </datafield>
  <datafield tag="690" ind1=" " ind2="7">
   <subfield code="a">Keywords Growth hormone, insulin-like growth factors, transforming growth factor β, vascular endothelial growth factor, epidermal growth factor, antagonist, angiotensin converting enzyme inhibition, protein kinase C inhibition, nephropathy, somatostatin analogue</subfield>
   <subfield code="2">nationallicence</subfield>
  </datafield>
  <datafield tag="856" ind1="4" ind2="0">
   <subfield code="u">https://doi.org/10.1007/s001250051515</subfield>
   <subfield code="q">text/html</subfield>
   <subfield code="z">Onlinezugriff via DOI</subfield>
  </datafield>
  <datafield tag="908" ind1=" " ind2=" ">
   <subfield code="D">1</subfield>
   <subfield code="a">research-article</subfield>
   <subfield code="2">jats</subfield>
  </datafield>
  <datafield tag="950" ind1=" " ind2=" ">
   <subfield code="B">NATIONALLICENCE</subfield>
   <subfield code="P">856</subfield>
   <subfield code="E">40</subfield>
   <subfield code="u">https://doi.org/10.1007/s001250051515</subfield>
   <subfield code="q">text/html</subfield>
   <subfield code="z">Onlinezugriff via DOI</subfield>
  </datafield>
  <datafield tag="950" ind1=" " ind2=" ">
   <subfield code="B">NATIONALLICENCE</subfield>
   <subfield code="P">100</subfield>
   <subfield code="E">1-</subfield>
   <subfield code="a">Flyvbjerg</subfield>
   <subfield code="D">A.</subfield>
   <subfield code="u">Medical Research Laboratory M (Diabetes and Endocrinology) and Medical Department M (Diabetes and Endocrinology), Institute of Experimental Clinical Research, University of Aarhus, Aarhus Community Hospital, Aarhus, Denmark, DK</subfield>
   <subfield code="4">aut</subfield>
  </datafield>
  <datafield tag="900" ind1=" " ind2="7">
   <subfield code="a">Metadata rights reserved</subfield>
   <subfield code="b">Springer special CC-BY-NC licence</subfield>
   <subfield code="2">nationallicence</subfield>
  </datafield>
  <datafield tag="898" ind1=" " ind2=" ">
   <subfield code="a">BK010053</subfield>
   <subfield code="b">XK010053</subfield>
   <subfield code="c">XK010000</subfield>
  </datafield>
  <datafield tag="949" ind1=" " ind2=" ">
   <subfield code="B">NATIONALLICENCE</subfield>
   <subfield code="F">NATIONALLICENCE</subfield>
   <subfield code="b">NL-springer</subfield>
  </datafield>
 </record>
</collection>
