ArticleEuropean journal of medical research2025
TXNIP regulates the proliferation of scar fibroblasts through oxidative stress.
Article in European journal of medical research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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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.
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Who cites it
1 citing paper in PubMed.
- Dynamic analysis of skin transcriptome in Xinjiang goats and functional verification ofVeterinary and animal science · 2026Article
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5 authors.
Funding
Abstract
BACKGROUND AND
objectiveHypertrophic scarring (HS) is a common fibroproliferative disorder that often develops following cutaneous injury and can cause significant psychological distress. Oxidative stress has been identified as a key driver of abnormal fibroblast activity, with thioredoxin-interacting protein (TXNIP) implicated in redox regulation. However, the specific role of TXNIP in scar fibroblast proliferation remains unclear. METHODS AND
resultsWestern blot and qPCR analysis showed that TXNIP expression in HS tissue was significantly higher than in normal skin. MTT, colony formation, and soft agar assays demonstrated that knocking out TXNIP significantly inhibited the viability and proliferation of HKF cells. Immunofluorescence and flow cytometry revealed that oxidative stress levels in HKF cells were markedly higher than in HSF cells, which were markedly reduced upon TXNIP silencing. Molecular docking predicted stable binding between TXNIP and thioredoxin (Trx) at residues Gly252 and Asn240, which was supported by co-immunoprecipitation results, suggesting that TXNIP regulates oxidative stress via direct interaction with Trx. Furthermore, in a murine model of hypertrophic scarring, TXNIP knockdown significantly attenuated scar formation.
conclusionTXNIP may promote the proliferation of scar fibroblasts by regulating oxidative stress, representing a potential therapeutic target for HS.
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