Expression of advanced glycation end products and their cellular receptor RAGE in diabetic nephropathy and nondiabetic renal disease.

@article{Tanji2000ExpressionOA,
  title={Expression of advanced glycation end products and their cellular receptor RAGE in diabetic nephropathy and nondiabetic renal disease.},
  author={Nozomu Tanji and Glen S. Markowitz and Chun-yan Fu and Thomas Kislinger and Akiko Taguchi and Monika Pischetsrieder and David Stern and Ann Marie Schmidt and Vivette D D'agati},
  journal={Journal of the American Society of Nephrology : JASN},
  year={2000},
  volume={11 9},
  pages={1656-66}
}
Advanced glycation end products (AGE) contribute to diabetic tissue injury by two major mechanisms, i.e., the alteration of extracellular matrix architecture through nonenzymatic glycation, with formation of protein crosslinks, and the modulation of cellular functions through interactions with specific cell surface receptors, the best characterized of which is the receptor for AGE (RAGE). Recent evidence suggests that the AGE-RAGE interaction may also be promoted by inflammatory processes and… CONTINUE READING

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References

Publications referenced by this paper.
Showing 1-10 of 30 references

Diabetes mellitus

JL Olson
Heptinstall’s Pathology of the Kidney, • 1998
View 1 Excerpt

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