2019
DOI: 10.1080/10715762.2019.1629586
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Role of redox imbalance and cytokines in mediating oxidative damage and disease progression of patients with rheumatoid arthritis

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Cited by 39 publications
(25 citation statements)
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“…Thus, an imbalance of cytokine network contributes to the development and progression of this autoimmune disease. In particular, TNF-α, IL-6, IL-1β and IFN-γ are considered to be disease promoting cytokines in RA [33,34]. In synovium, patients with RA had high frequencies of Th1 cells and of Th17 cells, which are thought to play a prominent pathogenic role in autoimmune arthritis.…”
Section: Discussionmentioning
confidence: 99%
See 1 more Smart Citation
“…Thus, an imbalance of cytokine network contributes to the development and progression of this autoimmune disease. In particular, TNF-α, IL-6, IL-1β and IFN-γ are considered to be disease promoting cytokines in RA [33,34]. In synovium, patients with RA had high frequencies of Th1 cells and of Th17 cells, which are thought to play a prominent pathogenic role in autoimmune arthritis.…”
Section: Discussionmentioning
confidence: 99%
“…In synovium, patients with RA had high frequencies of Th1 cells and of Th17 cells, which are thought to play a prominent pathogenic role in autoimmune arthritis. More recently, in plasma from RA patients, levels of IL-17, IL-23 and IFN-γ were significantly increased and correlated with a redox imbalance and oxidative damage [34]. Moreover, COMP, a specific serological marker which evaluates the articular cartilage degradation and its turnover, exerts an active role in inflammation.…”
Section: Discussionmentioning
confidence: 99%
“…Oxidative damages may aggravate mitochondrial dysfunctions and further accelerate the progression of sarcopenia. The hypothesis that mitochondrial dysfunctions could be involved in sarcopenia in RA patients could be drawn from the observation that oxidative stress was linked to chronic inflammation and RA [72]. The correlation between ROS production and the loss of handgrip strength in older women [73], the contribution of oxidative stress to skeletal muscle dysfunction in an animal models of RA [74] further corroborated this hypothesis.…”
Section: Mitochondrial Dysfunctionmentioning
confidence: 84%
“…This results in a vicious cycle of cell death and greater inflammation [29]. This ROS-inflammation axis has been studied in a wide array of inflammatory-based diseases, such as cardiac alterations [30][31][32], bone and joint diseases [33][34][35], neuronal and cerebral dysfunctions [28,29,36], bacterial infection [37], liver diseases [38], respiratory alterations [39,40] and cancer [41]. Furthermore, in T2D, the continuous presence of proinflammatory molecules causes diverse endocrine effects on the vasculature, and contributes to the development of micro-and macrovascular pathologies such as carotid atherosclerosis [21].…”
Section: Introductionmentioning
confidence: 99%