Roles of hydrogen sulfide in the pathogenesis of diabetes mellitus and its complications

Csaba Szabo

Research output: Contribution to journalArticle

93 Citations (Scopus)

Abstract

Significance: Diabetes and its complications represent a major socioeconomic problem. Recent Advances: Changes in the balance of hydrogen sulfide (H2S) play an important role in the pathogenesis of β-cell dysfunction that occurs in response to type 1 and type 2 diabetes. In addition, changes in H2S homeostasis also play a role in the pathogenesis of endothelial injury, which develop on the basis of chronically or intermittently elevated circulating glucose levels in diabetes. Critical Issues: In the first part of this review, experimental evidence is summarized implicating H2S overproduction as a causative factor in the pathogenesis of β-cell death in diabetes. In the second part of our review, experimental evidence is presented supporting the role of H2S deficiency (as a result of increased H2S consumption by hyperglycemic cells) in the pathogenesis of diabetic endothelial dysfunction, diabetic nephropathy, and cardiomyopathy. Future Directions: In the final section of the review, future research directions and potential experimental therapeutic approaches around the pharmacological modulation of H2S homeostasis in diabetes are discussed.

Original languageEnglish (US)
Pages (from-to)68-80
Number of pages13
JournalAntioxidants and Redox Signaling
Volume17
Issue number1
DOIs
StatePublished - Jul 1 2012

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Hydrogen Sulfide
Diabetes Complications
Medical problems
Homeostasis
Diabetic Cardiomyopathies
Diabetic Nephropathies
Type 1 Diabetes Mellitus
Type 2 Diabetes Mellitus
Cell Death
Pharmacology
Glucose
Wounds and Injuries
Cell death
Modulation
Direction compound
Therapeutics

ASJC Scopus subject areas

  • Biochemistry
  • Cell Biology
  • Molecular Biology
  • Physiology
  • Clinical Biochemistry

Cite this

Roles of hydrogen sulfide in the pathogenesis of diabetes mellitus and its complications. / Szabo, Csaba.

In: Antioxidants and Redox Signaling, Vol. 17, No. 1, 01.07.2012, p. 68-80.

Research output: Contribution to journalArticle

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