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Mild traumatic brain injury as a pathological process: Heliyon

Trx1’s activity is inhibited by binding to TXNIP and subsequent blocking of the active site [216]

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Observed outcomes include specific cellular and molecular endpoints such as: Enhanced fibroblast migration capacity Increased collagen and elastin deposition Modulation of pro-inflammatory and antioxidant mediators Altered transcriptional profiles related to tissue homeostasis, repair signaling, and stress response All reported observations derive exclusively from preclinical laboratory and animal studies and remain model-specific