Mitochondrial reactive oxygen species promote production of proinflammatory cytokines and are elevated in TNFR1-associated periodic syndrome (TRAPS)

By Ariel C. Bulua, A. Simon, R. Maddipati, M. Pelletier, Heiyoung Park, Kye-Young Kim, M. Sack, Daniel L. Kastner, R. Siegel. Journal of Experimental Medicine, 2011

844 citations recorded by the source corpus.

ROS generated by mitochondrial respiration are needed for optimal proinflammatory cytokine production in healthy cells, and are elevated in cells from patients with an autoinflammatory disorder.

Subfields: Immunology, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/78da45a3f3254f410b1f1aafb530457270be198b

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Immunology

1. M. Lamkanfi
2. G. Núñez
3. V. Dixit
4. L. Franchi
5. S. Reddy
6. Khiem A. Tran
7. V. Hornung
8. Asrar B. Malik

In Molecular Biology

1. M. Lamkanfi
2. G. Núñez
3. V. Dixit
4. Navdeep S. Chandel
5. L. Franchi
6. P. Schumacker
7. S. Reddy
8. Khiem A. Tran

Citations in the corpus

• Biological Activities of Reactive Oxygen and Nitrogen Species: Oxidative Stress versus Signal Transduction (2015, neutral): “[57] showed that”
• Redox Regulation of NLRP3 Inflammasomes: ROS as Trigger or Effector? (2015, positive): “Mitochondrial ROS (mtROS) Alternatively, there is an emerging role for mtROS in the mechanism of NLRP3 inflammasome activation (21,155).”
• Reactive Oxygen Species in Inflammation and Tissue Injury (2014, positive): “Monocytes and neutrophils isolated from TRAPS patients showed elevated baseline levels of mitochondrial ROS compared with healthy donors and also had constitutive and prolonged activation of JNK and p38 MAPK on LPS challenge (48).”
• TNF and TNF-receptors: From mediators of cell death and inflammation to therapeutic giants - past, present and future. (2014, background): “However, abnormal ER retention [131], mitochrondrial reactive oxygen species [132], ER stress, and the stress response to ‘‘unfolded’’ or aggregated proteins also contribute to TRAPS pathogenesis [133]; for review see [134].”
• ROS Function in Redox Signaling and Oxidative Stress (2014, background): “Interestingly, patients with tumor necrosis factor receptor-associated periodic syndrome (TRAPS) have heightened responsiveness to LPS, due to increased mitochondrial ROS production, which promotes inflammation, again suggesting that redox biology, and not oxidative stress, is regulating inflammator”
• Upregulated NLRP3 Inflammasome Activation in Patients With Type 2 Diabetes (2012, background): “Interestingly, patients with tumor necrosis factor receptor-associated periodic syndrome, an autoinflammatory disorder caused by missense mutations in the type 1 tumor necrosis factor receptor, have elevated mitochondrial ROS levels, which are responsible for the stronger inflammatory responses to L”
• Cutting Edge: Reactive Oxygen Species Inhibitors Block Priming, but Not Activation, of the NLRP3 Inflammasome (2011, background): “Furthermore, independent evidence also exists that ROS activate proinflammatory transcription factors (19, 20) and that ROS production positively regulates proinflammatory gene expression in various innate immune signaling pathways (14, 21).”