Selective inhibition of HSF1 expression in the heat shock pathway of keloid fibroblasts reduces excessive fibrosis in keloid.

The stress response following burns may be a crucial factor in keloid formation, yet the underlying pathological mechanisms remain to be elucidated. This study initially investigated how heat shock factor 1 (HSF1) and heat shock proteins (HSPs) within the heat shock pathway influence keloid fibrosis, providing insights into the role of the heat shock response in keloid development. This study aims to further elucidate the role of the heat shock pathway in keloid fibrosis and investigate the specific function of HSF1 within this pathway. This study focused on human keloid fibroblasts, examining the expression and regulatory role of HSF1 on HSPs under heat stress using immunohistochemistry, RNA interference, real-time fluorescent PCR, and Western blotting techniques. HSF1 was overexpressed in keloid fibroblasts and tissues compared to normal skin, and heat stress could further enhance HSF1 expression in both keloid tissues and fibroblasts. Functional inhibition of HSF1 significantly affected the expression of downstream HSPs in keloid fibroblasts, ultimately leading to the inhibition of keloid fibrosis. The heat shock pathway plays a crucial role in keloid fibrosis, with HSF1 as a key regulator influencing the expression of HSPs. Heat stress treatment of keloid fibroblasts offers an approach for investigating keloid formation.