重编程
线粒体
明胶
生物物理学
材料科学
PI3K/AKT/mTOR通路
细胞生物学
化学
生物化学
细胞凋亡
生物
细胞
作者
Shengjie Ge,Aidong Sun,Xinyu Zhou,Ping Niu,Yong Chen,Xiaotao Bao,Meng Yu,Zhenhua Zhong,Jingwu Sun,Guang Li
标识
DOI:10.1002/adma.202413371
摘要
Mitochondrial dysfunction, which is the primary mechanism underlying cisplatin-induced hearing loss, can potentially be mitigated by modulating the redox balance and reprogramming the energy metabolism to remodel mitochondrial homeostasis. Herein, N-acetyl-l-cysteine-derived carbonized polymer dots (NAC CPDs) are embedded into manganese porphyrin-doped metal-organic frameworks and encapsulated using a polydopamine (PDA) coating and gelatin methacryloyl (GelMA) hydrogel to afford functionalized nanozyme microcapsules. Owing to their injectability and adhesion properties, these microcapsules exhibit the advantages of prolonged retention in the middle ear and sustained release in the inner ear. The synergy between the manganese porphyrin and polymer dots results in excellent antioxidant properties. The developed nanozymes activate the PI3K-AKT pathway, reprogramming the energy supply mechanism, and inhibiting the oligomerization of BAX in mitochondria to prevent the leakage of mitochondrial DNA and cytochrome c. Therapeutic efficacy and related mechanisms are validated in vivo. Thus, this study on mitochondrial homeostasis remodeling by nanozyme microcapsules opens a new chapter in the treatment of hearing loss.
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