This study explores the dysregulated “mitophagy–apoptosis–inflammation” axis in hypertrophic scar (HS) pathophysiology and proposes a synergistic therapy to restore microenvironmental homeostasis. By targeting mitochondrial dysfunction and inflammatory signaling, the strategy enhances scar regression, providing a novel clinical approach for HS treatment. The findings highlight the potential of multiaxis modulation in improving therapeutic outcomes.

This study reveals that Mg-Ag anti-site defects in α-MgAgSb create staggered nanoscale zones, effectively scattering phonons while preserving carrier transport. Zn doping optimizes defect formation, achieving a high zT of ~0.45 at 200 K and ~0.75 average (200–400 K). A single-pair device demonstrates a 56 K temperature difference at 325 K, validating anti-site engineering for enhanced thermoelectric cooling.