New Insights for Oxidative Stress and Diabetes Mellitus

Abstract

The release of reactive oxygen species (ROS) and the generation of oxidative stress are considered critical factors for the pathogenesis of diabetes mellitus (DM), a disorder that is growing in prevalence and results in significant economic loss. New therapeutic directions that address the detrimental effects of oxidative stress may be especially warranted to develop effective care for the millions of individuals that currently suffer from DM. The mechanistic target of rapamycin (mTOR), silent mating type information regulation 2 homolog 1 (S. cerevisiae) (SIRT1), and Wnt1 inducible signaling pathway protein 1 (WISP1) are especially justified to be considered treatment targets for DM since these pathways can address the complex relationship between stem cells, trophic factors, impaired glucose tolerance, programmed cell death pathways of apoptosis and autophagy, tissue remodeling, cellular energy homeostasis, and vascular biology that greatly impact the biology and disease progression of DM. The translation and development of these pathways into viable therapies will require detailed understanding of their proliferative nature to maximize clinical efficacy and limit adverse effects that have the potential to lead to unintended consequences.

Figure 1

Oxidative stress in Diabetes Mellitus impacts pathways of stem cell proliferation, programmed cell death, and cellular energy homeostasis. Diabetes Mellitus (DM) leads to the development of oxidative stress and the release of reactive oxygen species (ROS). Novel proliferative pathways for targeting new treatments against DM and the complications of this disorder are the mechanistic target of rapamycin (mTOR), silent mating type information regulation 2 homolog 1 (S. cerevisiae) (SIRT1), and Wnt1 inducible signaling pathway protein 1 (WISP1). Each of these pathways is intimately connected through shared signal transduction mechanisms that can oversee stem cell proliferation, programmed cell death that involves apoptosis and autophagy, and cellular energy homeostasis that can affect mitochondrial function and insulin sensitivity.