去卵巢大鼠
凝聚
平衡
骨质疏松症
骨重建
雌激素
化学
医学
线粒体
骨密度
内科学
内分泌学
松质骨
骨病
骨愈合
老年性骨质疏松症
调节器
骨量减少
骨细胞
成骨细胞
更年期
代谢性骨病
合成代谢
还原(数学)
生物信息学
骨矿物
作者
S. X. Zhang,Yiwei Zeng,Sixu Zhang,Jiajing Zhou,Changsheng Liu,Xi Chen
出处
期刊:Nano Letters
[American Chemical Society]
日期:2025-10-26
卷期号:25 (44): 15854-15863
被引量:4
标识
DOI:10.1021/acs.nanolett.5c04029
摘要
Postmenopausal osteoporosis (PMOP) manifests as a systemic skeletal disorder arising from disrupted bone metabolic equilibrium, characterized by a marked reduction in bone mineral density and compromised microarchitectural integrity, ultimately leading to increased bone fragility and greater fracture susceptibility. Current delivery therapeutic strategies frequently fail to address mitochondrial dysfunction arising from estrogen depletion and senescence-associated processes. We developed a multifunctional coacervate system, in which peptide coacervates were used to encapsulate estradiol (E2) and subsequently coated by a metal-phenolic network (MPN), capable of concurrently modulating mitochondrial function and reconstructing bone homeostasis. The MPN-coated coacervates demonstrate microenvironment-responsive degradation within osteoporotic bone tissue. In ovariectomized aged mouse models, intravenous injection of these coacervates significantly increased bone volume in both the femur and vertebrae while mitigating side effects on the uterus. This unique therapeutic paradigm establishes a bidirectional regulatory mechanism that provides a promising strategy for comprehensive osteoporosis management.
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