ArticleMolecular biology reports2025
Nurr1 attenuates hepatic stellate cell activation by inhibiting EMT and cell cycle progression via interaction with Smad3.
Article in Molecular biology reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
Abstract
backgroundEpithelial–mesenchymal transition (EMT) plays a vital role in hepatic fibrosis, as hepatic stellate cells (HSCs) can undergo EMT during liver fibrogenesis. Our previous work indicated that overexpression of the orphan nuclear receptor Nurr1 (NR4A2) can inhibit HSC activation and ameliorate liver fibrosis. However, the underlying mechanism by which Nurr1 affects EMT in hepatic fibrosis remains unclear. METHODS AND
resultsHSC-T6 cells were transfected with either a Nurr1 overexpression plasmid or a small interfering RNA targeting Nurr1 to modulate Nurr1 levels. Transforming growth factor β1 (TGF-β1) was used to activate HSC-T6 cells. In vitro analyses showed that Nurr1 overexpression decreased α-smooth muscle actin (α-SMA) levels and increased E-cadherin (E-CAD) levels, whereas Nurr1 knockdown had the opposite effect. Consistently, Nurr1 overexpression reduced mRNA expression of EMT-related genes (α-SMA, Snail, Slug, and Smad3), while Nurr1 silencing elevated their expression. Flow cytometry revealed that Nurr1 overexpression increased the proportion of cells in S phase and reduced the G₂/M population, whereas Nurr1 knockdown also increased S-phase cells but led to accumulation in G₂/M phase. Chromatin immunoprecipitation (ChIP) assays demonstrated a significant enrichment of the Smad3 promoter in Nurr1-immunoprecipitated chromatin, indicating that Nurr1 directly binds to the Smad3 promoter.
conclusionsNurr1 suppresses HSC activation by downregulating EMT gene expression and modulating the cell cycle. Our findings suggest that Nurr1 inhibits the fibrogenic activation of HSCs, at least in part through transcriptional repression of EMT drivers (such as Smad3) and induction of S-phase cell cycle arrest.
Indexed as
Identifiers
40932596What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.