Nrf2, a novel molecular target to reduce type 1 diabetes associated secondary complications: The basic considerations

Abstract

Oxidative stress and inflammation are the mediators of diabetes and related secondary complications. Oxidative stress arises because of the excessive production of reactive oxygen species and diminished antioxidant production due to impaired Nrf2 activation, the master regulator of endogenous antioxidant. It has been established from various animal models that the transcription factor Nrf2 provides cytoprotection, ameliorates oxidative stress, inflammation and delays the progression of diabetes and its associated complications. Whereas, deletion of the transcription factor Nrf2 amplifies tissue level pathogenic alterations. In addition, Nrf2 also regulates the expression of numerous cellular defensive genes and protects against oxidative stress-mediated injuries in diabetes. The present review provides an overview on the role of Nrf2 in type 1 diabetes and explores if it could be a potential target for the treatment of diabetes and related complications. Further, the rationality of different agent's intervention has been discussed to mitigate organ damages induced by diabetes.

Keywords: Antioxidant response element; Diabetes; Kelch-like ECH-associated protein 1 NADPH quinone dehydrogenase 1; Nuclear factor erythroid 2 (NFE2)-related factor 2; Reactive oxygen species.