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Molecular pathways associated with oxidative stress in diabetes mellitus

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TLDR
Increased level of glyceraldehyde-3-P activates two major pro-oxidative pathways in diabetes, which causes the accumulation of glycolytic metabolites upstream, and this leads to excessive stimulation of other pro-oxygenative pathways such as hexosamine and polyol pathways.
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This article is published in Biomedicine & Pharmacotherapy.The article was published on 2018-12-01 and is currently open access. It has received 259 citations till now. The article focuses on the topics: Methylglyoxal & Protein kinase C.

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Oxidative Stress and Microvascular Alterations in Diabetic Retinopathy: Future Therapies.

TL;DR: This review focuses on analysing the sources and effects of oxidative stress and inflammation on vascular alterations and diabetic retinopathy development, and current and antioxidant therapies, together with new molecular targets, are postulated for diabetic Retinopathy treatment.
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Dexmedetomidine alleviated sepsis‑induced myocardial ferroptosis and septic heart injury.

TL;DR: The attenuation of sepsis-induced HO-1 overexpression and iron concentration, and the reduction of ferroptosis via enhancing GPX4, may be the major mechanisms via which Dex alleviates sepsi-induced myocardial cellular injury.
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Therapeutic potential of mushrooms in diabetes mellitus: Role of polysaccharides.

TL;DR: The present review discusses the pathophysiology of diabetes and, elaborates some potential mushroom species that are known to have antihyperglycemic activities and different mushroom polysaccharides modulating the composition of gut microflora in diabetic animal models have also been discussed.
References
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Journal ArticleDOI

Free radicals and antioxidants in normal physiological functions and human disease

TL;DR: Attention is focussed on the ROS/RNS-linked pathogenesis of cancer, cardiovascular disease, atherosclerosis, hypertension, ischemia/reperfusion injury, diabetes mellitus, neurodegenerative diseases, rheumatoid arthritis, and ageing.
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Biochemistry and molecular cell biology of diabetic complications

TL;DR: This integrating paradigm provides a new conceptual framework for future research and drug discovery in diabetes-specific microvascular disease and seems to reflect a single hyperglycaemia-induced process of overproduction of superoxide by the mitochondrial electron-transport chain.
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The pathobiology of diabetic complications: a unifying mechanism.

TL;DR: What was learned about the pathobiology of diabetic complications starting with that 1966 Science paper and continuing through the end of the 1990s are described, including a unified mechanism that links together all of the seemingly unconnected pieces of the puzzle.
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Oxidative stress and diabetic complications

TL;DR: Athrosclerosis and cardiomyopathy in type 2 diabetes are caused in part by pathway-selective insulin resistance, which increases mitochondrial ROS production from free fatty acids and by inactivation of antiatherosclerosis enzymes by ROS.

superoxide production blocks three pathways of hyperglycaemic damage

TL;DR: This paper showed that hyperglycaemia increases the production of reactive oxygen species inside cultured bovine aortic endothelial cells and that this increase in reactive oxygen can be prevented by an inhibitor of electron transport chain complex II, an uncoupler of oxidative phosphorylation, by uncoupling protein-1 and by manganese superoxide dismutase.
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