The electromechanical breast implant fixation device long-term suppress inflammatory responses to miligate its capsular contracture through a “self- regenerating antioxidant” ROS scavenging strategy

• A piezoelectric membrane was developed to prevent implant-induced capsular contracture. • The device combines barium titanate-enhanced PVDF with polydopamine to converts mechanical energy from breast motion into electric signals via piezoelectric coupling. • The device exhibits self- regenerating antioxidant capacity through electrically driven redox cycling of polydopamine. • The device modulates macrophage polarization and fibroblast activity, contributing to anti-inflammatory and anti-fibrotic effects. • This mechano-electrochemical strategy offers long-term, drug-free prevention of capsular contracture. Mechanical stress generated by breast motion can trigger inflammatory responses, contributing to capsular contracture around implants. Current strategies relying on antioxidant-loaded systems to scavenge ROS face challenges due to rapid activity attenuation, limiting long-term efficacy. This study designed a self- regenerating antioxidant breast implant fixation device using electrospun polyvinylidene fluoride (PVDF) membranes enhanced with barium titanate (BaTiO 3 ) nanoparticles to improve piezoelectricity. An antioxidant polydopamine (PDA) coating was applied to provide renewable antioxidant capacity. Under mechanical stimulation, the built-in piezoelectric output from the BaTiO 3 /PVDF membrane, generating local electrical cues that promote interfacial electron transfer. These electrons are proposed to convert oxidized quinone moieties in PDA back into reduced catechol/polyphenol groups, enabling regeneration of antioxidant activity. The membrane maintained over 80% scavenging efficiency after 10 oxidative cycles, demonstrating excellent long-term stability. In vitro, ultrasound-stimulated membranes inhibited fibroblast proliferation and migration, sustained ROS clearance for up to 72 h, and induced macrophage polarization toward the anti-inflammatory M2 phenotype. In a co-culture fibrosis model, collagen-associated markers decreased markedly, with hydroxyproline content maintained at a low level (0.985 μg/10 4 cells). In vivo subcutaneous implantation in mice showed effective suppression of collagen deposition and inflammation over 30 days, while maintaining normal skin thickness. Collectively, this electroactive membrane offers a self-regenerating solution to potentially mitigate capsular contracture via mechano-electrochemical synergy, serve as a proof-of-concept strategy for clinical application.