The DOI matches its Crossref record; 86 of the 86 references it cites were found in a registry or an index.
Mechanism of Generation of Oxidative Stress and Pathophysiology of Type 2 Diabetes Mellitus: How Are They Interlinked?
Abstract
Oxidative stress has been considered as a major hallmark for the pathogenesis and development of type 2 diabetes mellitus (T2DM), but still it is debatable whether it is a mere aggregation of inflammatory‐induced responses or clinical entity that underlies with various pathophysiological factors. In this regard, the latest studies have shown the increasing trends for the involvement of reactive oxygen species (ROS) and oxidative stress in the pathogenesis and development of T2DM. ROS are highly reactive species and almost all cellular components are chemically changed due to the influence of ROS that ultimately results in the production of lipid peroxidation. Lipid peroxidation is a major causative factor for the development of oxidative stress that leads to overt T2DM and its associated micro‐ and macro‐vascular complications. In this article, we have briefly described the role of various causative factors, transcriptional and metabolic pathways which are responsible to increase the production of oxidative stress, a most pivotal factor for the pathogenesis and development of T2DM. Therefore, we conclude that measurement of oxidative stress biomarkers may be one of the optional tool for the diagnosis and prediction of T2DM. Moreover, the key findings described in this article also provides a new conceptual framework for forthcoming investigations on the role of oxidative stress in pathogenesis of T2DM and drug discovery. J. Cell. Biochem. 118: 3577–3585, 2017. © 2017 Wiley Periodicals, Inc.
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Metadata
- Authors
- Rehman, K., & Akash, M. S. H.
- Venue
- Journal of Cellular Biochemistry
- Publisher
- Wiley
- Published
- 2017-05-31
- Volume
- 118
- Issue
- 11
- Pages
- 3577-3585
- ISSN
- 0730-2312 (ISSN-L)
- 1097-4644
- OpenAlex
- W2610612775
- Cited by
- 474
- References
- 86
- FWCI
- 19.40
- Type
- journal article
- Language
- en
- Open access
- closed
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