Abstract
Wound healing is a complex process that can lead to hypertrophic scarring (HS) when dysregulated. The role of lncRNAs in this process is increasingly recognized, yet the specific contributions of lncRNA STX17-AS1 require elucidation. This study investigated the expression of STX17-AS1, its regulatory effects on miR-145-5p, and downstream targets, highlighting its impact on wound repair and HS development. In a cohort of 20 HS patients and 20 matched controls, we assessed the expression of STX17-AS1, miR-145-5p and PDK1 via real-time PCR and immunohistochemistry. We correlated these expressions with wound characteristics and analysed their regulatory impact on the PI3K/AKT pathway, crucial for cellular proliferation and migration in wound healing. Elevated levels of STX17-AS1 and miR-145-5p in patient samples were correlated with larger wound areas and slower healing rates, suggesting the regulatory imbalance in scar formation. The negative correlation of PDK1 expression with age and its positive association with wound size underscored its relevance in wound repair mechanisms. Functional analysis confirmed the interaction between STX17-AS1 and miR-145-5p and modulation of PDK1, indicating the potential disruption of the PI3K/AKT pathway in the wound healing process. The study identified lncRNA STX17-AS1 as the significant mediator in wound healing, with aberrations in its pathway correlating with impaired healing and HS. The findings proposed lncRNA STX17-AS1 and miR-145-5p as molecular targets to enhance wound healing and prevent pathological scarring, offering a new avenue for therapeutic advances in wound management and regenerative medicine.