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Modulation of Nrf2 expression alters high glucose-induced oxidative stress and antioxidant gene expression in mouse mesangial cells.

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TLDR
Results indicated that Nrf2 and its downstream antioxidants, HO-1 and γ-GCS, are negative regulators of high glucose-induced ROS-related mouse mesangial cell dysfunction.
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This article is published in Cellular Signalling.The article was published on 2011-10-01. It has received 60 citations till now. The article focuses on the topics: Mesangial cell & Oxidative stress.

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Curcumin, inflammation, and chronic diseases: how are they linked?

TL;DR: Research to date suggests that chronic inflammation, oxidative stress, and most chronic diseases are closely linked, and the antioxidant properties of curcumin can play a key role in the prevention and treatment of chronic inflammation diseases.
Journal ArticleDOI

Mesangial cell biology.

TL;DR: Identification of biological responses of MCs that are not mediated by the renin-angiotensin system should help development of novel and effective therapeutic strategies to treat diseases characterized by MC pathology.
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Thioredoxin-interacting Protein Mediates High Glucose-induced Reactive Oxygen Species Generation by Mitochondria and the NADPH Oxidase, Nox4, in Mesangial Cells

TL;DR: TxNIP deficiency protects mesangial cells from HG-induced oxidative stress and increased collagen by blocking mitochondrial glucose metabolism, NADPH oxidase, and Nox4 by regulating the TCA cycle versus glycolytic glucose flux.
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Effect of Redox Modulating NRF2 Activators on Chronic Kidney Disease

TL;DR: Current findings on the renoprotective effects of naturally occurring NRF2 activators, including sulforaphane, resveratrol, curcumin, and cinnamic aldehyde are described, bringing a light of hope for ameliorating CKD progression by preventing oxidative stress and maintaining cellular redox homeostasis.
References
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Journal ArticleDOI

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.

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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Normalizing mitochondrial superoxide production blocks three pathways of hyperglycaemic damage

TL;DR: This work shows that hyperglycaemia increases the production of reactive oxygen species inside cultured bovine aortic endothelial cells and is prevented by an inhibitor of electron transport chain complex II, by an uncoupler of oxidative phosphorylation, by uncoupling protein-1 and by manganese superoxide dismutase.
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Keap1 represses nuclear activation of antioxidant responsive elements by Nrf2 through binding to the amino-terminal Neh2 domain

TL;DR: It is postulate that Keap1 and Nrf2 constitute a crucial cellular sensor for oxidative stress, and together mediate a key step in the signaling pathway that leads to transcriptional activation by this novel NRF2 nuclear shuttling mechanism.
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Role of free radicals in the neurodegenerative diseases: therapeutic implications for antioxidant treatment.

TL;DR: Little is known about the impact of dietary antioxidants upon the development and progression of neurodegenerative diseases, especially Alzheimer’s disease, but there are many attempts to develop antioxidants that can cross the blood-brain barrier and decrease oxidative damage.
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