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Journal ArticleDOI

Methylglyoxal induces apoptosis through activation of p38 MAPK in rat Schwann cells.

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TLDR
A potential role for MG is suggested in SC injury through oxidative stress-mediated p38 MAPK activation under diabetic conditions, and it may serve as a novel insight into therapeutic strategies for diabetic neuropathy.
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This article is published in Biochemical and Biophysical Research Communications.The article was published on 2004-07-30. It has received 98 citations till now. The article focuses on the topics: Methylglyoxal & Apoptosis.

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Citations
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Journal ArticleDOI

Methylglyoxal, a highly reactive dicarbonyl compound, in diabetes, its vascular complications and other age-related diseases

TL;DR: The mechanisms through which MGO is formed, its detoxification by the glyoxalase system, and its effect on biochemical pathways in relation to the development of diabetes, vascular complications of diabetes and other age-related diseases are summarized.
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The role of methylglyoxal and the glyoxalase system in diabetes and other age-related diseases.

TL;DR: The present review summarizes the mechanisms through which MGO is formed, its detoxification by the glyoxalase system and its effect on biochemical pathways in relation to the development of age-related diseases.
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The tandem of free radicals and methylglyoxal.

TL;DR: It is arrived at that a tight junction exists between methylglyoxal toxicity and free radical (particularly ROS) generation, though the toxicity of 1,2-dicarbonyl evolves even under anaerobic conditions, too.
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Stimulation of suicidal erythrocyte death by methylglyoxal.

TL;DR: In this article, the percentage of circulating erythrocytes exposing phosphatidylserine (PS) at the cell surface was found to increase with diabetes, and the phyto-serine was recognized, bound, engulfed and degraded by macrophages.
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Methylglyoxal Impairs the Insulin Signaling Pathways Independently of the Formation of Intracellular Reactive Oxygen Species

TL;DR: The data suggest that an increase in intracellular methylglyoxal content hampers a key molecule, thereby leading to inhibition of insulin-induced signaling in L6 muscle cells, and may contribute to the pathophysiology of diabetes in general.
References
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Journal ArticleDOI

Opposing Effects of ERK and JNK-p38 MAP Kinases on Apoptosis

TL;DR: The effects of dominant-interfering or constitutively activated forms of various components of the JNK-p38 and ERK signaling pathways demonstrated that activation of JNK and p38 and concurrent inhibition of ERK are critical for induction of apoptosis in these cells.
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Mammalian thioredoxin is a direct inhibitor of apoptosis signal-regulating kinase (ASK) 1.

TL;DR: Evidence that Trx is a negative regulator of ASK1 suggests possible mechanisms for redox regulation of the apoptosis signal transduction pathway as well as the effects of antioxidants against cytokine‐ and stress‐induced apoptosis.
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Induction of Apoptosis by ASK1, a Mammalian MAPKKK That Activates SAPK/JNK and p38 Signaling Pathways

TL;DR: Overexpression of ASK1 induced apoptotic cell death, andASK1 was activated in cells treated with tumor necrosis factor-α, and TNF-α-induced apoptosis was inhibited by a catalytically inactive form of AsK1.
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Pharmacology of methylglyoxal: formation, modification of proteins and nucleic acids, and enzymatic detoxification--a role in pathogenesis and antiproliferative chemotherapy.

TL;DR: The modification of nucleic acids and protein by methylglyoxal is a signal for their degradation and may have a role in the development of diabetic complications, atherosclerosis, the immune response in starvation, aging and oxidative stress.
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Isolation and functional characterization of Schwann cells derived from adult peripheral nerve

TL;DR: A method for procuring large, essentially pure populations of Schwann cell (ScC) populations from adult rat sciatic nerve at cell yields of greater than 2 x 10(4) cells/mg of starting nerve weight was developed and successfully applied to human tissue.
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