Working Together: Redox Signaling between the Endoplasmic Reticulum and Mitochondria

Siegenthaler, Kevin D; Sevier, Carolyn S.

doi:10.1021/acs.chemrestox.8b00379

Cited by 14 publications

(13 citation statements)

References 6 publications

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“…Crosstalk between these different ROS producing sites can result in a feed-forward loop amplifying an originally localized ROS signal. 91 Under physiologic conditions, ROS play an important role in BCR-mediated signaling and B cell fate decisions. ROS are produced in response to BCR stimulation 92,93 and can reversibly oxidize different signaling molecules such as protein tyrosine phosphatases SHP-2 and PTEN.…”

Section: Con S Equen Ce S Of D Is Rup Ted Me Tabolic Homeos Ta S Ismentioning

confidence: 99%

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The role of metabolic checkpoint regulators in B cell survival and transformation

Jellusova

2020

Immunological Reviews

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In response to mitogenic stimulation, B cells activate different pro-anabolic signaling pathways such as c-Myc-and mTORC1-dependent networks to satisfy the energetic demands of biomass synthesis and proliferation. In order to preserve viability and function, cell growth cannot progress unchecked and must be adjusted according to the availability of nutrients. Nutrient-sensing proteins such as AMPK antagonize mTORC1 activity in response to starvation. If pro-anabolic signaling pathways are aberrantly activated, B cells may lack the metabolic capacity to accommodate their energetic needs, which can lead to cell death. On the other hand, metabolic hyperactivation is a salient feature of cancer cells, suggesting that mechanisms exist, which allow B cells to cope with metabolic stress. The aim of this review is to discuss how B cells respond to a mismatch between energy supply and demand and what the consequences are of metabolic dysregulation in normal and malignant B cells. K E Y W O R D Sanabolism, autophagy, B cells, metabolic stress, mTORC1, senescence

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Section: Con S Equen Ce S Of D Is Rup Ted Me Tabolic Homeos Ta S Ismentioning

confidence: 99%

“…Additional sources of ROS include plasma membrane–associated NADPH oxidases (NOX) or dual oxidases (DUOX) (Figure 3). Crosstalk between these different ROS producing sites can result in a feed‐forward loop amplifying an originally localized ROS signal …”

Section: Consequences Of Disrupted Metabolic Homeostasismentioning

confidence: 99%

The role of metabolic checkpoint regulators in B cell survival and transformation

Jellusova

2020

Immunological Reviews

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“…Under reductive stress, abnormally increased electron pressure caused by increases of NADH, NADPH, and GSH leads to mitochondrial dysfunction [38]. Oxidative protein folding in the ER leads to the release of ROS via mitochondria-ER cross talk [44], which activates Nrf2 [46]. Nrf2-antioxidant response element signaling enhanced reductive stress in the human mutant protein aggregation cardiomyopathy (MPAC) [61].…”

Section: Current Insights Into the Dtt-induced Reductive Stressmentioning

confidence: 99%

“…Reductive stress also can result in ROS production, by controlling mitochondria to utilize the abundance of reducing equivalents or by perturbing protein folding and endoplasmic reticulum (ER) function [41][42][43]. ER, containing diverse systems to constrain ROS accumulation [44], is much more oxidizing than other cellular compartments and is more vulnerable to reductive stress [45]. In fact, there is a redox cross talk between mitochondria and ER [44].…”

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confidence: 99%

“…ER, containing diverse systems to constrain ROS accumulation [44], is much more oxidizing than other cellular compartments and is more vulnerable to reductive stress [45]. In fact, there is a redox cross talk between mitochondria and ER [44]. Oxidative protein folding in the ER leads to the release of ROS as by-products, which can be utilized to activate some transcriptional factors such as nuclear erythroid 2-related factor 2 (Nrf2) [46].…”

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confidence: 99%

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Reductive Stress-Induced Mitochondrial Dysfunction and Cardiomyopathy

Tao

et al. 2020

Oxidative Medicine and Cellular Longevity

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The goal of this review was to summarize reported studies focusing on cellular reductive stress-induced mitochondrial dysfunction, cardiomyopathy, dithiothreitol- (DTT-) induced reductive stress, and reductive stress-related free radical reactions published in the past five years. Reductive stress is considered to be a double-edged sword in terms of antioxidation and disease induction. As many underlying mechanisms are still unclear, further investigations are obviously warranted. Nonetheless, reductive stress is thought to be caused by elevated levels of cellular reducing power such as NADH, glutathione, and NADPH; and this area of research has attracted increasing attention lately. Albeit, we think there is a need to conduct further studies in identifying more indicators of the risk assessment and prevention of developing heart damage as well as exploring more targets for cardiomyopathy treatment. Hence, it is expected that further investigation of underlying mechanisms of reductive stress-induced mitochondrial dysfunction will provide novel insights into therapeutic approaches for ameliorating reductive stress-induced cardiomyopathy.

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