European journal of medical research · 2025
TXNIP regulates the proliferation of scar fibroblasts through oxidative stress.
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Gong Wenbo, Zhang Songtao, Zhang Runfang, Li Yanqing, Zhai Xiaomei
Аннотация
BACKGROUND AND OBJECTIVE: Hypertrophic 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 RESULTS: Western 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.
CONCLUSION: TXNIP may promote the proliferation of scar fibroblasts by regulating oxidative stress, representing a potential therapeutic target for HS.
METHODS AND RESULTS: Western 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.
CONCLUSION: TXNIP may promote the proliferation of scar fibroblasts by regulating oxidative stress, representing a potential therapeutic target for HS.