1999
DOI: 10.1002/1529-0131(199911)42:11<2430::aid-anr22>3.0.co;2-6
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Expression of the thioredoxin-thioredoxin reductase system in the inflamed joints of patients with rheumatoid arthritis

Abstract: The data demonstrate significantly increased concentrations of TRX in the SF and ST of RA patients when compared with the levels in patients with other joint diseases. Evidence is presented that the local environment in the rheumatic joint contributes to increased TRX production. Based on its growth-promoting and cytokine-like properties, it is proposed that increased expression of TRX contributes to the disease activity in RA.

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Cited by 109 publications
(52 citation statements)
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“…Indeed, increased TF + MP levels correlate with hypercoagulability in endotoxemic mice (79), and extracellular TRX levels are significantly elevated in plasma of sepsis patients (80). Similarly, P2RX7 signaling is implicated in rheumatoid arthritis (81), and high levels of extracellular TRX (82,83) as well as of TF + MPs (84) are detected in the synovial fluids of patients. Notably, the TRXR inhibitor auranofin is efficacious in the treatment of rheumatoid arthritis.…”
Section: Discussionmentioning
confidence: 99%
“…Indeed, increased TF + MP levels correlate with hypercoagulability in endotoxemic mice (79), and extracellular TRX levels are significantly elevated in plasma of sepsis patients (80). Similarly, P2RX7 signaling is implicated in rheumatoid arthritis (81), and high levels of extracellular TRX (82,83) as well as of TF + MPs (84) are detected in the synovial fluids of patients. Notably, the TRXR inhibitor auranofin is efficacious in the treatment of rheumatoid arthritis.…”
Section: Discussionmentioning
confidence: 99%
“…In addition, TrxR is involved in the redox activity of RAW264.7 macrophages [54][55][56]. Our interest in examining the binding of gold complexes, and possibly Au NPs, to TrxR was derived in part from the contribution that these interactions may make to their anti-arthritic activity [18,19].…”
Section: Thioredoxin Reductase Binding Studiesmentioning
confidence: 99%
“…Both Trx and TrxR are over-expressed in synovial cells or fluid of RA patients [18,19]. Inhibition of TrxR by gold drugs has attracted interest due to the presence of a selenocysteine residue at its active site, and the greater affinity of Au(I) for selenol groups compared to thiols [20,21].…”
Section: Introductionmentioning
confidence: 99%
“…Another important antioxidant system that would suffer from TrxR inhibition is that of the mammalian peroxiredoxins, which all require functional Trx for regeneration (16). Furthermore, cytokine functions of extracellular Trx, as well as increased Trx and TrxR levels in some tumor cell lines and in synovial fluid or tissue of patients suffering from rheumatoid arthritis (10,17), argue for targeting of TrxR as a possible therapeutic approach in certain diseases. In fact, TrxR is inactivated by several compounds in clinical use, including 1,3-bis-(2-chloro-ethyl)-1-nitrosourea (BCNU) (18), anticancer platinum compounds (19), antiarthritic gold compounds (20,21), and immunostimulatory dinitrohalobenzenes (22).…”
mentioning
confidence: 99%