ArticleCellular and molecular life sciences : CMLS2022
A circular RNA, circPTPN14, increases MYC transcription by interacting with FUBP1 and exacerbates renal fibrosis.
Article in Cellular and molecular life sciences : CMLS, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 11 citations in OpenAlex.
- circ_0002456/FUS interaction inhibits NF-κB signaling to attenuate DNA damage and inflammatory responses in hDPSCs.Stem cell research & therapy · 2025Article
- Facilitation of diabetic wound healing by far upstream element binding protein 1 through augmentation of dermal fibroblast activity.Acta diabetologica · 2025Article
- RfxCas13d-mediated inhibition ofRenal failure · 2024Article
- Large-Scale Alternative Polyadenylation-Wide Association Studies to Identify Putative Cancer Susceptibility Genes.Cancer research · 2024Article
- CircRNAs: versatile players and new targets in organ fibrosis.Cell communication and signaling : CCS · 2023Review
- circPTPN14 promotes renal fibrosis through its interaction with FUBP1 to enhance MYC transcription.Cellular and molecular life sciences : CMLS · 2023Article
- Isoliensinine Attenuates Renal Fibrosis and Inhibits TGF-β1/Smad2/3 Signaling Pathway in Spontaneously Hypertensive Rats.Drug design, development and therapy · 2023Article
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Authors and funding
13 authors at 4 institutions in 1 country.
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Abstract
Fibrosis is a relentlessly progressive and irreversible cause of organ damage, as in chronic kidney disease (CKD), but its underlying mechanisms remain elusive. We found that a circular RNA, circPTPN14, is highly expressed in human kidneys with biopsy-proved chronic interstitial fibrosis, mouse kidneys subjected to ischemia/reperfusion (IR) or unilateral ureteral obstruction (UUO), and TGFβ1-stimulated renal tubule epithelial cells (TECs). The intrarenal injection of circPTPN14 shRNA alleviated the progression of fibrosis in kidneys subjected to IR or UUO. Knockdown of circPTPN14 in TECs inhibited TGFβ1-induced expression of profibrotic genes, whereas overexpressing circPTPN14 increased the profibrotic effect of TGFβ1. The profibrotic action of circPTPN14 was ascribed to an increase in MYC transcription. The binding of circPTPN14 to the KH3 and KH4 domains of far upstream element (FUSE) binding protein 1 (FUBP1) enhanced the interaction between FUBP1 and FUSE domain, which was required for the initiation of MYC transcription. In human kidneys (n = 30) with biopsy-proved chronic interstitial fibrosis, the expression of circPTPN14 positively correlated with MYC expression. Taken together these studies show a novel mechanism in the pathogenesis of renal fibrosis, mediated by circPTPN14, which can be a target in the diagnosis and treatment of CKD.
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