Evaluation of levels of oxidative stress as a potential biomarker in patients with rheumatoid arthritis

Kaushik, Madhulika; De, Soumita; Kundu, Sunanda; Ghosh, Parasar; Chatterjee, Suparna; Chatterjee, Mitali

doi:10.4103/jfmpc.jfmpc_2412_20

Cited by 3 publications

(4 citation statements)

References 23 publications

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“…In previous studies, increased ROS levels have been reported in patients with RA (24,25); therefore, the present study investigated the relationship between SNP rs16917496 and ROS levels in patients with RA. ROS levels were higher in the CC genotype carriers (1011.500±536.426 vs. 548.616±190.508, P=0.032, Fig.…”

Section: Genementioning

confidence: 95%

Polymorphisms in microRNA binding site of SET8 regulate the risk of rheumatoid arthritis

et al. 2023

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Rheumatoid arthritis (RA) is a complex, heterogeneous, progressive and long-term autoimmune disease characterized by symmetrical joint inflammation and bone erosion. The etiology of RA is unclear, but its pathogenesis is associated with oxidative stress and inflammatory cytokines. Single nucleotide polymorphisms (SNPs) in the microRNA (miRNA)-binding sites modify the development of rheumatic disease by regulating the expression of target genes. The present study investigated whether SNPs in the miRNA binding site in the 3' untranslated region (3'-UTR) of SET domain containing lysine methyltransferase) 8 (SET8) and Keratin 81 (KRT81), namely rs16917496 and rs3660, respectively, were associated with the occurrence of RA. The polymerase chain reaction-ligase detection reaction assay showed that the distribution frequencies of the CC genotype (P=0.025) of SNP rs16917496 in SET8 were significantly higher in patients with RA than in healthy controls, which indicated that the CC genotype was associated with an increased risk of RA. SET8 expression in the blood samples of CC genotype carriers was lower than that of TT genotype carriers. Moreover, the CC genotype carriers exhibited higher reactive oxygen species (ROS) levels (1011.500±536.426 vs. 548.616±190.508, P=0.032) and lower interleukin-10 (IL-10) levels (P<0.001). The present study demonstrated that SNP rs16917496 in the 3'-UTR of SET8 was a predictor of RA risk and may regulate RA development by mediating expression of SET8, thereby regulating the levels of ROS and IL-10.

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Section: Genementioning

confidence: 95%

Polymorphisms in microRNA binding site of SET8 regulate the risk of rheumatoid arthritis

et al. 2023

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“…With this device, it is possible to determine the redox balance in the sample using the d-ROMs Fast (measurement of free radicals) and PAT (measurement of antioxidant power) tests and, therefore, to calculate the OSI. In most cases, the study of OS in various diseases is conducted on blood samples taken from a peripheral vein; however, in this way, only the “general” oxidative state of the patient is analyzed [ 53 , 54 , 55 , 56 , 58 , 59 , 60 , 61 , 62 ].…”

Section: Methodsmentioning

confidence: 99%

Measurement of Oxidative Stress Index (OSI) in Penile Corpora Cavernosa and Peripheral Blood of Peyronie’s Disease Patients: A Report of 49 Cases

Paulis,

De Giorgio

et al. 2024

Metabolites

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Peyronie’s disease (PD) is a chronic inflammatory disease affecting the penile albuginea. Oxidative stress (OS) is important for the development of the disease; therefore, it seemed interesting to us to directly measure OS at both the site of the disease and in peripheral blood. For a precise OS study, it is necessary to evaluate not only the single results of the total oxidant status (TOS) and total antioxidant status (TAS) but also their ratio: OS index (OSI) (arbitrary unit) = TOS/TAS × 100. This study included 49 PD patients examined and diagnosed in our Peyronie’s care center and a control group of 50 cases. We collected blood samples from both the penis and a vein in the upper extremity; we used d-ROMs and PAT-test (FRAS kit) for OS measurement. Pearson’s study found a statistical correlation between penile OSI values and PD plaque volumes: p-value = 0.002. No correlation was found between systemic OSI values and PD plaque volumes: p-value = 0.27. Penile OSI values were significantly reduced after the elimination of the PD plaque (p < 0.00001). The mean value of the penile OSI indices in the PD patients after plaque elimination corresponded to 0.090 ± 0.016 (p = 0.004). The comparison between the penile OSI values of the PD patients (with plaque elimination) and the control group revealed no statistically significant differences (p = 0.130). The absence of a correlation between Peyronie’s plaque volume and systemic OSI values indicates that it is preferable to carry out the OS study by taking a sample directly from the site of the disease. By carrying out a penile OSI study, it would be possible to obtain a precise plaque-volume-dependent oxidative marker. Even if the study did not demonstrate any correlation between OSI indices and anxious–depressive state, we detected a high prevalence of anxiety (81.6%) and depression (59.1%) in PD patients.

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“…For example, excessive ROS is toxic to non-FSLs and triggers ferroptosis in these cells; however, ROS accumulation has a pro-proliferative and pro-survival role in FSLs. Several studies have attempted to explore alternative methods to assess the disease activity and prognosis of RA by monitoring the levels of ROS, mtDNA, and other markers of oxidative stress ( 46 , 54 , 55 ). However, further studies and explorations are still needed to address the use of oxidative stress markers in the treatment of RA.…”

Section: Association Between Ferroptosis and Ramentioning

confidence: 99%

“…alternative methods to assess the disease activity and prognosis of RA by monitoring the levels of ROS, mtDNA, and other markers of oxidative stress (46,54,55). However, further studies and explorations are still needed to address the use of oxidative stress markers in the treatment of RA.…”

Section: Lipid Peroxidation and Oxidative Stress In Ramentioning

confidence: 99%

Ferroptosis as an emerging target in rheumatoid arthritis

Zhao,

Tang,

Wang

et al. 2023

Front. Immunol.

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Rheumatoid arthritis (RA) is an autoimmune disease of unknown etiology. Due to the rise in the incidence rate of RA and the limitations of existing therapies, the search for new treatment strategies for RA has become a global focus. Ferroptosis is a novel programmed cell death characterized by iron-dependent lipid peroxidation, with distinct differences from apoptosis, autophagy, and necrosis. Under the conditions of iron accumulation and the glutathione peroxidase 4 (GPX4) activity loss, the lethal accumulation of lipid peroxide is the direct cause of ferroptosis. Ferroptosis mediates inflammation, oxidative stress, and lipid oxidative damage processes, and also participates in the occurrence and pathological progression of inflammatory joint diseases including RA. This review provides insight into the role and mechanism of ferroptosis in RA and discusses the potential and challenges of ferroptosis as a new therapeutic strategy for RA, with an effort to provide new targets for RA prevention and treatment.

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Evaluation of levels of oxidative stress as a potential biomarker in patients with rheumatoid arthritis

Cited by 3 publications

References 23 publications

Polymorphisms in microRNA binding site of SET8 regulate the risk of rheumatoid arthritis

Polymorphisms in microRNA binding site of SET8 regulate the risk of rheumatoid arthritis

Measurement of Oxidative Stress Index (OSI) in Penile Corpora Cavernosa and Peripheral Blood of Peyronie’s Disease Patients: A Report of 49 Cases

Ferroptosis as an emerging target in rheumatoid arthritis

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