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In this study, we identified pericytes as novel fibrotic effector cells in IVDD, contributing to fibrosis through activation of the TGF\u2010\u03b2 signaling pathway. To address this, we developed a microgel platform (MMS@TRP) designed to specifically inhibit pericyte activation and pro\u2010fibrotic transition. MMS@TRP was constructed by integrating a tetrahedral framework nucleic acid (tFNA)\u2010based nanocarrier (TRP), which encapsulates a miR\u201021 inhibitor and is conjugated with a pericyte\u2010targeting peptide (pPB), onto tannic acid (TA)\u2010based metal\u2010phenolic network (MPN)\u2010functionalized gelatin methacryloyl microspheres (GelMA MS). This microgel system protects TRP from enzymatic degradation by nucleases while facilitating its pH\u2010sensitive release. The early\u2010stage release of TRP from MMS@TRP ensures targeted delivery of the miR\u201021 inhibitor to pericytes, suppressing pericyte proliferation, migration, and myofibroblast transition by blocking the TGF\u2010\u03b2 signaling pathway. Simultaneously, sustained TA release provides prolonged protection to nucleus pulposus cells (NPCs) through reactive oxygen species (ROS) scavenging, mitochondrial preservation, and anti\u2010inflammatory effects. 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