
NCBI . NLM . NIH . GOV {
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Title[redir]:
Mitochondrial reactive oxygen species drive proinflammatory cytokine production - PMC
Description:
Recent work indicates that mitochondrial ROS act via several pathways to elicit proinflammatory cytokines in human and mouse cells.
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Keywords {๐}
mtros, production, activation, ros, doi, inflammasome, pubmed, google, scholar, pmc, proinflammatory, inflammatory, mitochondria, cytokine, mitochondrial, cytokines, levels, nlrp, traps, autophagy, free, tnf, bulua, response, caspase, article, nlm, reactive, cells, increase, zhou, ilฮฒ, cell, nakahira, ncbi, search, oxygen, species, diseases, normal, signaling, lps, inflammasomes, med, syndrome, human, mechanisms, inflammation, transcriptional, protein,
Topics {โ๏ธ}
nf-ฮบbโdependent transcriptional activation reactive oxygen species pmc beta search mitochondrial respiratory-chain diseases lc3-deficient macrophages generated mrna-binding protein tristetraprolin bone marrow-derived macrophages il-1ฮฒ secretion induced autophagy-related protein lc3b pmc copyright notice modulate irf3-dependent induction lps-induced il-6 production ipaf/nlrc4 inflammasome respond publisher site pdf proinflammatory cytokine production inflammasome-dependent stimuli lps ros-driven human diseases innate immune activation highly reactive nature tumor necrosis factor proinflammatory cytokine activation previous study showing cytokine-based therapies mitochondrial dna mediated deregulated inflammatory responses inflammatory cytokine subsets inflammasome-independent roles redox regulator superoxide defective mitochondrial biogenesis proinflammatory transcriptional networks phosphatase activity defines regulate transcription directly conformational alteration induced free radic nlrp3-dependent stimuli inactivate mapk phosphatases cytokine gene transcription united states government deleterious effects caused mutant mefs correlated treat cryopyrinopathies caused amplification loop depends signal transduction properties redox-sensitive cysteines high cardiovascular risk pmc disclaimer elicit proinflammatory cytokines interferon response factor ros-dependent manner mechanisms linking ros
Questions {โ}
- , MAPK phosphatases) of cytokine gene transcription (B)?
- Consequently, a pressing question is, how do NLRP3-dependent stimuli inhibit autophagy?
- Defective mitochondrial biogenesis: a hallmark of the high cardiovascular risk in the metabolic syndrome?
- For example, are MAPK phosphatases only inhibited in the presence of higher levels of mtROS that presumably accumulate at later stages of an inflammatory response?
- Oxidative stress, inflammation, and cancer: how are they linked?
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