Transcriptional control of glyoxalase 1 by Nrf2 provides a stress-responsive defence against dicarbonyl glycation.

@article{Xue2012TranscriptionalCO,
  title={Transcriptional control of glyoxalase 1 by Nrf2 provides a stress-responsive defence against dicarbonyl glycation.},
  author={Mingzhan Xue and Naila Rabbani and Hiroshi Momiji and Precious Imbasi and Mammdouh M. Anwar and Neil R. Kitteringham and B. Kevin Park and Tomokazu Souma and Takashi Moriguchi and Masayuki Yamamoto and Paul J Thornalley},
  journal={The Biochemical journal},
  year={2012},
  volume={443 1},
  pages={
          213-22
        }
}
Abnormal cellular accumulation of the dicarbonyl metabolite MG (methylglyoxal) occurs on exposure to high glucose concentrations, inflammation, cell aging and senescence. It is associated with increased MG-adduct content of protein and DNA linked to increased DNA strand breaks and mutagenesis, mitochondrial dysfunction and ROS (reactive oxygen species) formation and cell detachment from the extracellular matrix. MG-mediated damage is countered by glutathione-dependent metabolism by Glo1… 
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Reappraisal of putative glyoxalase 1-deficient mouse and dicarbonyl stress on embryonic stem cells in vitro.
TLDR
Surprisingly, gene trapping by the International Mouse Knockout Consortium (IMKC) to generate putative Glo1 knockout mice produced a mouse line with the phenotype characterised as normal and healthy, and it was found that prolonged exposure of mouse ESCs in culture to high concentrations of MG and/or hypoxia led to low-level increase in GlO1 copy number.
Methylglyoxal disturbs the expression of antioxidant, apoptotic and glycation responsive genes and triggers programmed cell death in human leukocytes.
Methylglyoxal-induced dicarbonyl stress in aging and disease: first steps towards glyoxalase 1-based treatments.
Dicarbonyl stress is the abnormal accumulation of dicarbonyl metabolites leading to increased protein and DNA modification contributing to cell and tissue dysfunction in aging and disease. It is…
Alpha lipoic acid attenuates ER stress and improves glucose uptake through DNAJB3 cochaperone
TLDR
Results are supportive of an essential role of DNAJB3 as a molecular target through which ALA alleviates ER stress and improves glucose uptake and the effect of ALA on insulin-stimulated glucose uptake is significantly reduced.
Activation of Nrf2 attenuates carbonyl stress induced by methylglyoxal in human neuroblastoma cells: Increase in GSH levels is a critical event for the detoxification mechanism.
Interplay among Oxidative Stress, Methylglyoxal Pathway and S-Glutathionylation
TLDR
The data reported here stress the need for further studies aimed at understanding what role the evolutionary-conserved MGO formation and metabolism can play in cell signaling and response to OxS conditions, the aberration of which may importantly contribute to the pathogenesis of diseases associated to elevated OxS.
Resveratrol upregulates Nrf2 expression to attenuate methylglyoxal-induced insulin resistance in Hep G2 cells.
TLDR
Resveratrol significantly elevated glucose uptake and protected against MG-induced insulin resistance in Hep G2 cells and activated the extracellular signal-regulated kinase (ERK) pathway but not the p38 or c-Jun N-terminal kinases (JNK) pathways, subsequently leading to Nrf2 nuclear translocation and elevation of HO-1 and glyoxalase expression levels.
Mangiferin Upregulates Glyoxalase 1 Through Activation of Nrf2/ARE Signaling in Central Neurons Cultured with High Glucose
TLDR
It is demonstrated that Glo-1 was greatly downregulated in central neurons exposed to chronic high glucose, which is expected to lead the formation of AGEs and oxidative stress damages.
Regulation of Mitochondrial Functions by Transcription Factor NRF2
TLDR
The biology and role of NRF2 in regulating mitochondrial functions are discussed and current strategies used to targetNRF2 are summarized in order to confer protection against pulmonary disorders linked to mitochondrial dysfunction.
SIRT1 participates in the response to methylglyoxal-dependent glycative stress in mouse oocytes and ovary.
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