A review of the molecular mechanisms of hyperglycemia-induced free radical generation leading to oxidative stress

Habib Yaribeygi, Stephen Atkin, Amirhossein Sahebkar

Research output: Contribution to journalArticle

14 Citations (Scopus)

Abstract

The prevalence of diabetes is growing worldwide with an increasing morbidity and mortality associated with the development of diabetes complications. Free radical production is a normal biological process that is strictly controlled and has been shown to be important in normal cellular homeostasis, and in the bodies response to pathogens. However, there are several mechanisms leading to excessive free radical production that overcome the normal protective quenching mechanisms. Studies have shown that many of the diabetes complications result from excessive free radical generation and oxidative stress, and it has been shown that chronic hyperglycemia is a potent inducer for free radical production, generated through several pathways and triggering multiple molecular mechanisms. An understanding of these processes may help us to improving our preventive or therapeutic strategies. In this review, the major molecular pathways involved in free radical generation induced by hyperglycemia are described.

Original languageEnglish
JournalJournal of Cellular Physiology
DOIs
Publication statusAccepted/In press - 1 Jan 2018

Fingerprint

Oxidative stress
Hyperglycemia
Free Radicals
Oxidative Stress
Medical problems
Diabetes Complications
Biological Phenomena
Pathogens
Quenching
Homeostasis
Morbidity
Mortality

Keywords

  • cytochrome P450 enzyme system
  • diabetes complications
  • free radicals
  • hyperglycemia
  • NADPH oxidase
  • oxidative stress

ASJC Scopus subject areas

  • Physiology
  • Clinical Biochemistry
  • Cell Biology

Cite this

A review of the molecular mechanisms of hyperglycemia-induced free radical generation leading to oxidative stress. / Yaribeygi, Habib; Atkin, Stephen; Sahebkar, Amirhossein.

In: Journal of Cellular Physiology, 01.01.2018.

Research output: Contribution to journalArticle

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