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RESEARCH PAPER / 2026-04-17

Biomimetic KeMA hydrogel encapsulating CAP-EVs-MEF2C for inhibiting inflammation and senescence in intervertebral disc degeneration.

Jian-Bin Guan, Kai-Yuan Lin, Shan-Xi Wang, Ying-Guang Wang, Ling-Jiang Li, Ren-Ji Wang, Peng Zou, Xiao-Fan Bai, Si-Bo Wang, Liang Yan, Yuan-Ting Zhao, Xiao-Jun Yu

Department of Spine Surgery, Honghui Hospital, Xi'an Jiaotong University, Shaanxi Key Laboratory of Spine Bionic Treatment, No.555 Youyi East Road, South Gate, Beilin District, Shaanxi, 710054, Xi'an, China.Department of Spine Surgery, Honghui Hospital, Xi'an Jiaotong University, Shaanxi Key Laboratory of Spine Bionic Treatment, No.555 Youyi East Road, South Gate, Beilin District, Shaanxi, 710054, Xi'an, China. · pubmed

Abstract

This study aimed to develop a KeMA hydrogel encapsulating cartilage-affinity peptide (CAP)-modified extracellular vesicles (EVs) derived from MEF2C-overexpressing macrophages (KeMA@CAP-EVs-MEF2C) to modulate the MEF2C/P21/CDK2 axis, attenuating inflammation in cartilaginous endplate chondrocytes (CEPCs) and cellular senescence in nucleus pulposus cells (NPCs) to slow intervertebral disc degeneration (IVDD) progression. Single-cell RNA sequencing (scRNA-seq) identified MEF2C as a key regulator, upregulating p21 and suppressing CDK2 to reduce inflammation and cellular senescence. CAP-modified EVs within KeMA hydrogel demonstrated enhanced delivery and sustained-release properties. In vivo validation showed effective mitigation of cellular senescence and structural restoration in IVDD. This biomimetic system offers a promising strategy for IVDD treatment, emphasizing its targeting efficiency, biocompatibility, and sustained therapeutic benefits.

The following analysis is generated by AI and may contain errors. It is separate from the authors’ abstract and is not peer review.

Research summary

The study claims that the KeMA hydrogel encapsulating CAP-EVs-MEF2C can inhibit inflammation and cellular senescence in intervertebral disc degeneration. This research addresses mechanisms related to cellular senescence and inflammation, which are key factors in the aging process and age-related degeneration.

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