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D-ribose induces nephropathy through RAGE-dependent NF-κB inflammation.

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  • 1Integrated Laboratory of Traditional Chinese Medicine and Western Medicine, Peking University First Hospital, Beijing, 100034, People's Republic of China.

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High D-ribose levels in diabetes accelerate protein glycation, forming advanced glycation end products (AGEs). This study reveals D-ribose triggers kidney dysfunction through the receptor of AGEs (RAGE)-dependent NF-κB pathway, suggesting a mechanism for diabetic nephropathy.

Keywords:
AGEsDiabetesKidneyRAGE

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Area of Science:

  • Biochemistry
  • Nephrology
  • Endocrinology

Background:

  • Aberrantly high D-ribose levels are found in type II diabetic patients.
  • D-ribose glycates proteins faster than D-glucose, producing advanced glycation end products (AGEs).
  • AGE accumulation is linked to impaired renal function, but mechanisms remain unclear.

Purpose of the Study:

  • To investigate if D-ribose induces renal dysfunction via the receptor of AGEs (RAGE)-dependent nuclear factor kappa B (NF-κB) signaling pathway.
  • To elucidate the molecular mechanisms underlying D-ribose-induced nephropathy.

Main Methods:

  • In vivo studies using mice treated with D-ribose.
  • In vitro studies using human mesangial cells.
  • Immunohistochemistry, western blot, immunofluorescent staining, co-immunoprecipitation, and gene silencing (RAGE).

Main Results:

  • D-ribose administration lowered blood glucose and improved insulin tolerance in vivo.
  • Mice receiving D-ribose showed increased urine nitrogen and creatinine excretion, severe renal damage, and elevated kidney levels of NF-κB, AGEs, and RAGE.
  • In vitro, D-ribose induced NF-κB activation, AGEs, and RAGE accumulation in mesangial cells.
  • RAGE silencing blocked D-ribose-induced NF-κB phosphorylation.

Conclusions:

  • D-ribose induces inflammation via the RAGE-dependent NF-κB pathway.
  • This RAGE-dependent NF-κB activation is a potential triggering mechanism for D-ribose-induced nephropathy in type II diabetes.