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Glomerular Endothelial Cell Stress and Cross-Talk With Podocytes in Early
corrected Diabetic Kidney Disease
#MMPMID29629372
Daehn IS
Front Med (Lausanne)
2018[]; 5
(?): 76
PMID29629372
show ga
Diabetic kidney disease (DKD) is one of the major causes of morbidity and
mortality in diabetic patients and also the leading single cause of end-stage
renal disease in the United States. A large proportion of diabetic patients
develop DKD and others don't, even with comparable blood glucose levels,
indicating a significant genetic component of disease susceptibility. The
glomerulus is the primary site of diabetic injury in the kidney, glomerular
hypertrophy and podocyte depletion are glomerular hallmarks of progressive DKD,
and the degree of podocyte loss correlates with severity of the disease. We know
that chronic hyperglycemia contributes to both microvascular and macrovascular
complications, as well as podocyte injury. We are beginning to understand the
role of glomerular endothelial injury, as well as the involvement of reactive
oxygen species and mitochondrial stress, which play a direct role in DKD and in
other diabetic complications. There is, however, a gap in our knowledge that
links genetic susceptibility to early molecular mechanisms and proteinuria in
DKD. Emerging research that explores glomerular cell's specific responses to
diabetes and cell cross-talk will provide mechanistic clues that underlie DKD and
provide novel avenues for therapeutic intervention.
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