Inhibition of suppressor of cytokine signaling 1 mediates the profibrotic effect of TWEAK/Fn14 signaling on kidney cells

Chen, Jingyun; Jia, Fangyan; Ren, Kaixuan; Luo, Mai; Min, Xiaoyun; Wang, Ping; Xiao, Shengxiang; Xia, Yumin

doi:10.1016/j.cellsig.2020.109615

Cited by 11 publications

(10 citation statements)

References 34 publications

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“…The main source of soluble TWEAK in inflammatory tissue is macrophages / monocytes 11 . These data show that the TWEAK / Fn14 pathway makes significant contributions to inflammation in tissues and indicates that excessive or persistent upregulation of this pathway contributes significantly to the pathogenesis of some inflammatory diseases such as SLE and RA [12][13][14][15] .…”

Section: Introductionmentioning

confidence: 70%

Tweak Levels in Rheumatic Inflammatory Diseases

Kehribar¹

2021

jamp

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The objective of this study is to investigate and compare serum levels of tumor necrosis factor-like weak inducer of apoptosis (TWEAK) in rheumatoid arthritis (RA), systemic lupus erythematosus (SLE) and Behçet's disease. Patients with a diagnosis of RA (n = 20), SLE (n = 20) and Behçet's disease (n = 20) and a healthy control group (n = 19) were included in our study. Disease activity indexes, erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) levels were recorded in the patient groups. Serum TWEAK levels were measured with available commercial enzyme linked immunosorbent assay kits. The serum TWEAK levels were significantly higher in all patient groups compared to the control group. However, no significant difference was found in paired comparisons among patient groups. When the patients with high disease activity scores were compared to patients with low disease activity scores in RA, SLE and Behçet's disease subgroups, there was no significant difference in terms of TWEAK levels. Hypertension, atherosclerosis, diabetes mellitus and smoking had no effect on serum TWEAK levels. In correlation analysis, although serum TWEAK levels showed a significant negative correlation with age (r = -0.361, p = 0.005), there was no significant correlation with body mass index (BMI), ESR, and CRP levels. In RA, SLE and Behçet's disease, although different inflammatory pathways and different cytokine release patterns play a role in their pathogenesis, the similar increase in serum TWEAK levels and the absence of a relationship with the disease activity scores reflecting the last stage of inflammation may indicate that the TWEAK / Fn14 pathway plays a role in earlier stages where the inflammatory pathways have not differentiated yet.

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Section: Introductionmentioning

confidence: 70%

Tweak Levels in Rheumatic Inflammatory Diseases

Kehribar¹

2021

jamp

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“…The main source of soluble TWEAK in inflammatory tissue is macrophages / monocytes [15]. These data show that the TWEAK / Fn14 pathway makes significant contributions to inflammation in tissues and indicates that excessive or persistent upregulation of this pathway contributes significantly to the pathogenesis of some rheumatic inflammatory and infective diseases [16][17][18][19][20].…”

Section: Introductionmentioning

confidence: 76%

Assessment of serum TWEAK levels in patients with familial Mediterranean fever

Yavuzbilge¹,

Okuyucu²,

Civil³

et al. 2021

Journal of Surgery and Medicine

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“…TWEAK contributes to kidney inflammation by promoting cytokine production in different renal cells (tubular cells, mesangial cells, podocytes and fibroblasts) through canonical and non-canonical NF-jB activations [48]. Furthermore, TWEAK activation also contributes to renal fibrosis in LN, a final common pathway leading to ESRD [49]. Recently, TWEAK has been proposed as a promising biomarker of active LN in patients with SLE [20,21,[30][31][32][33][34][35][36].…”

Section: Discussionmentioning

confidence: 99%