Endoplasmic Reticulum Stress-Targeted Antibacterial Heterojunctions for Periodontal Tissue Regeneration

Heterojunction materials are used to achieve non-ROS-dependent disruption of the bacterial respiratory chain. This heterojunction composite consisting of CoSe, Ti₃C₂ MXene and taurine captures electrons derived from H₂O₂ in the infected microenvironment and transfers them to heme on the bacterial membrane. This process causes electron accumulation inside bacteria, impairs respiratory chain function and blocks ATP synthesis, ultimately leading to bacterial death.

Heterojunction materials are applied for immune reprogramming of the inflammatory microenvironment. Inside cells, the material exhibits multiple enzyme-mimicking activities to efficiently scavenge reactive oxygen species (ROS) and concurrently activate the anabolic synthesis of selenoproteins such as GPX1. By inhibiting the PERK-CHOP signaling pathway, the material effectively alleviates endoplasmic reticulum stress, drives macrophage polarization from the pro-inflammatory M1 phenotype to the repair-promoting M2 phenotype, and fundamentally breaks the vicious cycle of "endoplasmic reticulum stress-ROS-inflammation".

Heterojunction materials are utilized to restore and regenerate periodontal bone homeostasis. The material not only suppresses RANKL-induced osteoclast differentiation but also markedly promotes osteogenic differentiation of human periodontal ligament cells. In animal models, the material reduces alveolar bone resorption and facilitates periodontal tissue repair through synergistic antibacterial effects and microenvironment modulation.
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