The crosstalk between Nrf2 and NF-κB pathways in coronary artery disease: Can it be regulated by SIRT6?

Casper, Eman

doi:10.1016/j.lfs.2023.122007

Cited by 26 publications

(12 citation statements)

References 139 publications

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“…Among the limitations is the limited number of specific markers of oxidative stress, which could contribute to a better understanding of the results. This is significant because an increase in oxidative stress is an important factor related to the activation of the NF-κB signaling pathway [ 52 ].…”

Section: Discussionmentioning

confidence: 99%

Effects of Branched-Chain Amino Acids on the Inflammatory Response Induced by LPS in Caco-2 Cells

Garcia,

Makiyama,

Sampaio

et al. 2024

Metabolites

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Branched-chain amino acids (BCAA) are essential for maintaining intestinal mucosal integrity. However, only a few studies have explored the role of BCAA in the modulation of intestinal inflammation. In this study, we investigated in vitro effects of BCAA on the inflammatory response induced by lipopolysaccharide (LPS) (1 µg/mL) in Caco-2 cells. Caco-2 cells were assigned to six groups: control without BCAA (CTL0), normal BCAA (CTL; 0.8 mM leucine, 0.8 mM isoleucine, and 0.8 mM valine); leucine (LEU; 2 mM leucine), isoleucine (ISO; 2 mM isoleucine), valine (VAL; 2 mM valine), and high BCAA (LIV; 2 mM leucine, 2 mM isoleucine, and 2 mM valine). BCAA was added to the culture medium 24 h before LPS stimulation. Our results indicated that BCAA supplementation did not impair cell viability. The amino acids leucine and isoleucine attenuated the synthesis of IL-8 and JNK and NF-kB phosphorylation induced by LPS. Furthermore, neither BCAA supplementation nor LPS treatment modulated the activity of glutathione peroxidase or the intracellular reduced glutathione/oxidized glutathione ratio. Therefore, leucine and isoleucine exert anti-inflammatory effects in Caco-2 cells exposed to LPS by modulating JNK and NF-kB phosphorylation and IL-8 production. Further in vivo studies are required to validate these findings and gather valuable information for potential therapeutic or dietary interventions.

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Section: Discussionmentioning

confidence: 99%

Effects of Branched-Chain Amino Acids on the Inflammatory Response Induced by LPS in Caco-2 Cells

Garcia,

Makiyama,

Sampaio

et al. 2024

Metabolites

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“…Inhibition of XPO1-mediated oxaliplatin-induced HMGB nuclear export increases HCT116 decreases cell death t has been reported previously that cytosolic HMGB1 and HMGB2 can regulate apoptosis through the activation of NF-kB 30,31 and down regulation of Nrf2 32,33 , suggesting that inhibition of HMGB1 and HMGB2 secretion from the nucleus might ameliorate the oxaliplatin-mediated increase in cell death of HCT116 by preventing the down-regulation of Nrf2, a master controller of both ROS and lipid hydroperoxide detoxi cation pathways 32,33 required to prevent ferroptosis 34 . Inhibition of the nuclear exporter XPO1 with 75 nM Selinexor, did indeed signi cantly reduce oxaliplatin-mediated HMGB1 (Fig.…”

Section: Inhibition Of Oxaliplatin Induced Crt Translocation From The...mentioning

confidence: 92%

Ferroptosis and HMGB2 induced calreticulin translocation required for immunogenic cell death are controlled by the nuclear exporter XPO1

Blair,

Fan,

Gillespie

et al. 2024

Preprint

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Cisplatin and oxaliplatin cause the secretion of high mobility group box 1 (HMGB1) from cancer cells, which is necessary for initiation of immunogenic cell death (ICD). Calreticulin (CRT) translocation from the endoplasmic reticulum to the plasma membrane is also required; oxaliplatin induces this translocation but cisplatin does not. We have discovered that oxaliplatin causes the secretion of both HMGB1 and HMGB2 from the nucleus into the extracellular milieu. We previously showed that cisplatin mediated secretion of HMGB1 is controlled by the nuclear exporter XPO1 (chromosomal maintenance 1; CRM1). We now find that XPO1 regulates oxaliplatin mediated secretion of both HMGB1 and HMGB2. XPO1 inhibition causes nuclear accumulation of both proteins, inhibition of oxaliplatin-mediated ferroptosis of colon cancer cells, and inhibition of CRT translocation to the plasma membrane of lung and colon cancer cells. Incubation of cancer cells with cell targeted (CT)-HMGB2 confirmed that HMGB2 is responsible for translocation of CRT to the plasma membrane. CT-HMGB2 is three orders of magnitude more potent than oxaliplatin at inducing CRT translocation. Inhibition of HMGB1 and HMGB2 secretion and/or their activation of nuclear factor-kappa B (NF-kB) has potential utility for treating cardiovascular, and neurodegenerative diseases; whereas CT-HMGB2 could augment therapeutic approaches to cancer treatment.

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“…Under physiological conditions, Nrf2 and nuclear factor kappa-B (NF-κB) signaling pathways are mutually coordinated to maintain cellular homeostasis ( 42 ). Under pathological conditions, oxidative stress can mediate the occurrence of inflammatory reactions, and excessive ROS can activate IκB kinase (IκK), inducing phosphorylation of its inhibitor IκB and leading to proteasomal degradation of IκB protein.…”

Section: The Relationship Between Sci With Oxidative Stressmentioning

confidence: 99%

“…This results in nuclear translocation of NF-κB and activation of downstream genes such as IL-6 and TNF-α ( 43 ). Nrf2 can inhibit the degradation of IκB-α, thereby blocking NF-κB nuclear translocation and the transcription of pro-inflammatory genes ( 42 ). Conversely, NF-κB can enhance the recruitment of histone deacetylase 3 to the antioxidant response element region, leading to inhibition of Nrf2 activity and hindrance of ARE gene transcription, thereby suppressing antioxidant responses ( 44 ).…”

Section: The Relationship Between Sci With Oxidative Stressmentioning

confidence: 99%

Research progress on the inhibition of oxidative stress by teriparatide in spinal cord injury

Ai,

Xiong,

Deng

et al. 2024

Front. Neurol.

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Spinal cord injury (SCI) is currently a highly disabling disease, which poses serious harm to patients and their families. Due to the fact that primary SCI is caused by direct external force, current research on SCI mainly focuses on the treatment and prevention of secondary SCI. Oxidative stress is one of the important pathogenic mechanisms of SCI, and intervention of oxidative stress may be a potential treatment option for SCI. Teriparatide is a drug that regulates bone metabolism, and recent studies have found that it has the ability to counteract oxidative stress and is closely related to SCI. This article summarizes the main pathological mechanisms of oxidative stress in SCI, as well as the relationship between them with teriparatide, and explores the therapeutic potential of teriparatide in SCI.

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The crosstalk between Nrf2 and NF-κB pathways in coronary artery disease: Can it be regulated by SIRT6?

Cited by 26 publications

References 139 publications

Effects of Branched-Chain Amino Acids on the Inflammatory Response Induced by LPS in Caco-2 Cells

Effects of Branched-Chain Amino Acids on the Inflammatory Response Induced by LPS in Caco-2 Cells

Ferroptosis and HMGB2 induced calreticulin translocation required for immunogenic cell death are controlled by the nuclear exporter XPO1

Research progress on the inhibition of oxidative stress by teriparatide in spinal cord injury

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