Piezo1-A Key Pathogenic Factor in Breast Implant-Associated Capsular Contracture.

BACKGROUND

Capsular contracture (CC) remains one of the most common complications following breast implant surgery, yet its underlying mechanisms are not fully clarified. The mechanosensitive ion channel Piezo1 has been implicated in fibrotic processes across various organs; however, its role in breast implant-associated fibrosis remains unknown.

OBJECTIVE

This study aimed to investigate the expression and functional significance of Piezo1 in the pathogenesis of breast implant-associated capsular contracture.

METHODS

Using a murine silicone-implanted model, we analyzed expression of Piezo1 during capsule formation. Human capsular tissues (normal and contracted) were examined for Piezo1 expression. A lipoteichoic acid (LTA)-induced contracture model was employed to assess the therapeutic effect of GsMTx4, a specific Piezo1 inhibitor. Evaluations included histology, immunofluorescence, and Western blot analysis.

RESULTS

Piezo1 expression was significantly upregulated during early capsule formation in mice, showing a correlating with collagen deposition and capsular thickening. Patients contracted capsules exhibited markedly higher Piezo1 levels compared to normal capsules. In the LTA-induced contracture model, pharmacological inhibition of Piezo1 with GsMTx4 substantially reduced collagen deposition, capsular thickness, and Piezo1 expression levels.

CONCLUSION

Our findings establish Piezo1 as a critical mediator in the pathogenesis of breast implant-associated capsular contracture. The channel's dynamic expression and the efficacy of its inhibition highlight its pivotal role in the fibrotic process. Piezo1 represents a novel target, offering a promising therapeutic strategy for preventing this challenging complication.

LEVEL OF EVIDENCE V: This journal requires that authors assign a level of evidence to each article. For a full description of these Evidence-Based Medicine ratings, please refer to the Table of Contents or the online Instructions to Authors www.springer.com/00266 .