Cell biology of diabetic kidney disease

Yashpal S. Kanwar, Shigeru Akagi, Lin Sun, Baibaswata Nayak, Ping Xie, Jun Wada, Sumant S. Chugh, Farhad R. Danesh

Research output: Contribution to journalShort survey

11 Citations (Scopus)

Abstract

In large part cellular dysfunctions induced by chronic hyperglycemia are similar in type-1 and -2 diabetes. In both instances chronic hyperglycemia induces injury to a multitude of organs by affecting various target cells. The cells affected may include those derived from of epithelial or mesenchymal progenitors; and attimes hyperglycemia may induce phenotypic changes with epithelial-mesenchymal transformation. In the majority of target cells the high-glucose ambience activates various intracellular pathways that are similar except for minor exceptions that are related to the selective expression of various molecules in a given cell type. Keeping in perspective a common paradigm applicable to most of the cells, a brief discussion of different hyperglycemia-induced cellular events pertaining to various pathways is described in this review. They include fluxes of glucose intermediaries in various cellular metabolic pathways, generation of advanced glycation end products (AGEs) and their extra- and intracellular effects, the role of protein kinase C, transforming growth factor-β, guanosine triphosphate-binding proteins and reactive oxygen species (ROS) in various cellular signaling events. The latter, i.e., ROS, may be central to several intracellular pathways and modulate various events in a reciprocal manner. The information compiled under various subtitles of this synopsis is derived from an enormous amount of literature data summarized in several recent excellent reviews, and thus further reading of them is suggested to gather detailed comprehensive information on each of the subjects.

Original languageEnglish
Pages (from-to)e100-e110
JournalNephron - Experimental Nephrology
Volume101
Issue number3
DOIs
Publication statusPublished - Nov 1 2005

Keywords

  • Advanced glycation end products
  • Guanosine triphosphate-binding proteins
  • Hyperglycemia
  • Protein kinase C
  • Reactive oxygen species

ASJC Scopus subject areas

  • Physiology
  • Genetics
  • Nephrology

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  • Cite this

    Kanwar, Y. S., Akagi, S., Sun, L., Nayak, B., Xie, P., Wada, J., Chugh, S. S., & Danesh, F. R. (2005). Cell biology of diabetic kidney disease. Nephron - Experimental Nephrology, 101(3), e100-e110. https://doi.org/10.1159/000087339