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Comparative Proteomic Analysis of Whole Kidney, Medulla, and Cortical Tubules in Diabetic Pathogenesis of Kidney Injury in Mice
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Comparative Proteomic Analysis of Whole Kidney, Medulla, and Cortical Tubules in Diabetic Pathogenesis of Kidney Injury in Mice

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Trail and kidney disease

Corina Lorz1, Alberto Benito, Alvaro C Ucero

  • 1Renal and Vascular Research Laboratory, Fundacion Jimenez Diaz-UAM, Madrid, Spain. clorz@ciemat.es

Frontiers in Bioscience (Landmark Edition)
|March 11, 2009
PubMed

Insights

Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) plays a role in diabetic nephropathy. Increased TRAIL expression and high glucose sensitize kidney cells to apoptosis, contributing to disease progression.

Area of Science:

  • Immunology
  • Nephrology
  • Cell Biology

Background:

  • Diabetic nephropathy (DN) is a major complication of diabetes, characterized by progressive kidney damage.
  • TNF-related apoptosis-inducing ligand (TRAIL) is a cytokine implicated in cellular apoptosis and inflammation.

Purpose of the Study:

  • To investigate the role of TRAIL and its receptors in the pathogenesis of diabetic nephropathy.
  • To explore the influence of hyperglycemia and inflammatory cytokines on TRAIL expression and function in renal cells.

Main Methods:

  • Analysis of TRAIL and receptor expression in renal cells from patients with diabetic nephropathy.
  • In vitro studies using cultured renal cells exposed to high glucose and inflammatory cytokines.

Main Results:

  • Glomerular and tubulointerstitial expression of TRAIL is elevated in diabetic nephropathy.
  • Proinflammatory cytokines enhance TRAIL expression in tubular cells.
  • High glucose sensitizes renal tubular cells to TRAIL-induced apoptosis.
  • Osteoprotegerin (OPG), a decoy receptor, is upregulated in diabetic nephropathy and counteracts TRAIL's effects.

Conclusions:

  • TRAIL and its receptors are involved in the pathogenesis of diabetic nephropathy.
  • Hyperglycemia and inflammation exacerbate TRAIL-mediated apoptosis in the kidney.
  • OPG may act as a protective mechanism against TRAIL-induced damage in diabetic nephropathy.

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