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Reactive oxygen species: sources, consequences and targeted therapy in type 2 diabetes
Abstract
Oxidative stress has been considered as a central mediator in the progression of diabetic complication. The intracellular reactive oxygen species (ROS) leads to oxidative stress and it is raised from the mitochondria as well as by activation of five major pathways: increased polyol pathway flux, activation of protein kinase C (PKC) pathway, increased formation of advanced glycation end products (AGEs), over activity of hexosamine pathway and increased production of angiotensin II. The increased ROS through these pathways leads to β-cell dysfunction and insulin resistance, responsible for cell damage and death. This review not only highlights the sources of ROS production and their involvement in the progression of diabetes, but also emphasizes on pharmacological interventions and targeting of ROS in type 2 diabetes. This review summarizes the ROS as potential therapeutic targets, based on a putative mechanism in the progression of the diabetes. It also summarizes current knowledge of ROS activation in type 2 diabetes as well as ROS as a possible target for its treatment. Eventually, it would be a promising target for various strategies and drugs to modulate ROS levels in diabetes.
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“Therefore, ROS is capable to directly damage β cells, promoting apoptosis, or it can indirectly regulate insulin signaling pathway to inhibit the function of β cells (82, 83).”
From Diabetes and Sarcopenic Obesity: Pathogenesis, Diagnosis, and Treatments (2020) · cites this paper as [83]
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Metadata
- Authors
- Panigrahy, S. K., Bhatt, R., & Kumar, A.
- Affiliations
- Guru Ghasidas Vishwavidyalaya (IN)
- National Institute of Technology Raipur (IN)
- Corresponding author
- Bhatt, Renu
- Kumar, Awanish
- Venue
- Journal of Drug Targeting
- Publisher
- Informa UK Limited
- Published
- 2016-07-19
- Volume
- 25
- Issue
- 2
- Pages
- 93-101
- ISSN
- 1026-7158 (ISSN-L)
- 1061-186X
- 1029-2330
- OpenAlex
- W2468238510
- Cited by
- 103
- References
- 142
- Citations by year
- 2026: 3 · 2025: 10 · 2024: 12 · 2023: 10 · 2022: 20 · 2021: 11 · 2020: 11 · 2019: 8 · 2018: 6 · 2017: 11 · 2016: 1
- FWCI
- 0.89
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Journal of drug targeting (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Clinical Biochemistry › Advanced Glycation End Products research
- Health Sciences › Medicine › Physiology (medical) › Nitric Oxide and Endothelin Effects
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
- Keywords
- reactive oxygen species, oxidative stress, type 2 diabetes, polyol pathway, protein kinase C, advanced glycation end products, hexosamine biosynthetic pathway, angiotensin II, beta-cell dysfunction, insulin resistance, diabetes complications, antioxidant therapy
- MeSH terms
- Diabetes Mellitus, Type 2, Humans, Insulin Resistance, Reactive Oxygen Species
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