ArticleInflammation research : official journal of the European Histamine Research Society ... [et al.]2021
Inhibition of fibroblast growth factor-inducible 14 attenuates experimental tubulointerstitial fibrosis and profibrotic factor expression of proximal tubular epithelial cells.
Article in Inflammation research : official journal of the European Histamine Research Society ... [et al.], 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- TWEAK/Fn14 Signaling Drives Oxidative Cardiac Injury in Systemic Lupus Erythematosus: Evidence From Patient Biomarker Studies, Lupus Mouse Models, and Cardiomyocyte Assays.Arthritis & rheumatology (Hoboken, N.J.) · 2026Article
- 3D Humanized Bioprinted Tubulointerstitium Model to Emulate Renal Fibrosis In Vitro.Advanced healthcare materials · 2024Article
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Authors and funding
11 authors.
Funding
Abstract
BACKGROUND AND
aimAs a proinflammatory cytokine, tumor necrosis factor-like weak inducer of apoptosis (TWEAK) participates in the progression of renal fibrosis by binding to its receptor, fibroblast growth factor-inducible 14 (Fn14). However, the effect of Fn14 inhibition on tubular epithelial cell-mediated tubulointerstitial fibrosis remains unclear. This study aimed to elucidate the role of TWEAK/Fn14 interaction in the development of experimental tubulointerstitial fibrosis as well as the protective effect of Fn14 knockdown on proximal tubular epithelial cells.
methodsA murine model of unilateral ureteral obstruction was constructed in both wild-type and Fn14-deficient BALB/c mice, followed by observation of the tubulointerstitial pathologies.
resultsFn14 deficiency ameliorated the pathological changes, including inflammatory cell infiltration and cell proliferation, accompanied by reduced production of profibrotic factors and extracellular matrix deposition. In vitro experiments showed that TWEAK dose-dependently enhanced the expression of collagen I, fibronectin, and α-smooth muscle actin in proximal tubular epithelial cells. Interestingly, TWEAK also upregulated the expression levels of Notch1/Jagged1. Fn14 knockdown and Notch1/Jagged1 inhibition also mitigated the effect of TWEAK on these cells.
conclusionsIn conclusion, TWEAK/Fn14 signals contributed to tubulointerstitial fibrosis by acting on proximal tubular epithelial cells. Fn14 inhibition might be a therapeutic strategy for protecting against renal interstitial fibrosis.
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