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

*Corresponding author for this work

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 (US)
JournalNephron - Experimental Nephrology
Volume101
Issue number3
DOIs
StatePublished - Nov 1 2005

Fingerprint

Diabetic Nephropathies
Cell Biology
Hyperglycemia
Reactive Oxygen Species
Glucose
Advanced Glycosylation End Products
Epithelial-Mesenchymal Transition
Transforming Growth Factors
Guanosine Triphosphate
Metabolic Networks and Pathways
Type 1 Diabetes Mellitus
Type 2 Diabetes Mellitus
Protein Kinase C
Reading
Carrier Proteins
Wounds and Injuries

Keywords

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

ASJC Scopus subject areas

  • Physiology
  • Genetics
  • Nephrology

Cite this

Kanwar, Y. S., Akagi, S., Sun, L., Nayak, B., Xie, P., Wada, J., ... Danesh, F. R. (2005). Cell biology of diabetic kidney disease. Nephron - Experimental Nephrology, 101(3). https://doi.org/10.1159/000087339
Kanwar, Yashpal S ; Akagi, Shigeru ; Sun, Lin ; Nayak, Baibaswata ; Xie, Ping ; Wada, Jun ; Chugh, Sumant S. ; Danesh, Farhad R. / Cell biology of diabetic kidney disease. In: Nephron - Experimental Nephrology. 2005 ; Vol. 101, No. 3.
@article{55d55e1460664a56bb16f77560342aa8,
title = "Cell biology of diabetic kidney disease",
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.",
keywords = "Advanced glycation end products, Guanosine triphosphate-binding proteins, Hyperglycemia, Protein kinase C, Reactive oxygen species",
author = "Kanwar, {Yashpal S} and Shigeru Akagi and Lin Sun and Baibaswata Nayak and Ping Xie and Jun Wada and Chugh, {Sumant S.} and Danesh, {Farhad R.}",
year = "2005",
month = "11",
day = "1",
doi = "10.1159/000087339",
language = "English (US)",
volume = "101",
journal = "Experimental Nephrology",
issn = "0028-2766",
publisher = "S. Karger AG",
number = "3",

}

Kanwar, YS, Akagi, S, Sun, L, Nayak, B, Xie, P, Wada, J, Chugh, SS & Danesh, FR 2005, 'Cell biology of diabetic kidney disease', Nephron - Experimental Nephrology, vol. 101, no. 3. https://doi.org/10.1159/000087339

Cell biology of diabetic kidney disease. / Kanwar, Yashpal S; Akagi, Shigeru; Sun, Lin; Nayak, Baibaswata; Xie, Ping; Wada, Jun; Chugh, Sumant S.; Danesh, Farhad R.

In: Nephron - Experimental Nephrology, Vol. 101, No. 3, 01.11.2005.

Research output: Contribution to journalShort survey

TY - JOUR

T1 - Cell biology of diabetic kidney disease

AU - Kanwar, Yashpal S

AU - Akagi, Shigeru

AU - Sun, Lin

AU - Nayak, Baibaswata

AU - Xie, Ping

AU - Wada, Jun

AU - Chugh, Sumant S.

AU - Danesh, Farhad R.

PY - 2005/11/1

Y1 - 2005/11/1

N2 - 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.

AB - 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.

KW - Advanced glycation end products

KW - Guanosine triphosphate-binding proteins

KW - Hyperglycemia

KW - Protein kinase C

KW - Reactive oxygen species

UR - http://www.scopus.com/inward/record.url?scp=27544483644&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=27544483644&partnerID=8YFLogxK

U2 - 10.1159/000087339

DO - 10.1159/000087339

M3 - Short survey

VL - 101

JO - Experimental Nephrology

JF - Experimental Nephrology

SN - 0028-2766

IS - 3

ER -