时间标签：数据日期 2026-11-05 · 生成时间 2026-11-05 05:30（Asia/Shanghai）｜ 检索窗口 PubMed edat 2026/11/02 – 2026/11/06 ｜ 情报发生日期 2026-11-05
研究问题
These data focus on P-MM@Ps-CeO2’s ability to restore mitochondrial homeostasis, a marker of curative objective in HF, through the recruitment of PGAM5- induced fission and oxidant-antioxidant imbalance.P-MM@Ps-CeO2 ameliorates HF in miceFigure 6A depicts a flowchart illustrating the experiment in the DOX-induced HF model, where P-MM@Ps-CeO2 raised survival to 90% compared to 60% in DOX controls (Fig.；Objective image screening revealed an outstanding 50% decline in the fluorescence intensity of both PGAM5 and Constitutional DRP1 in cardiomyocytes from the P-MM@Ps-CeO2 group compared to the DOX group (P < 0.01), substantiating the positional subsiding of these fission proteins.To assess the immunomodulatory consequences, macrophage polarization was assessed (Fig. 7G, H).；Imaging was performed with a laser-scanning confocal microscope (SP8, Leica Microsystems, Germany) using a 63 × oil-immersion objective to obtain high-resolution fluorescence images of individual mitochondria.
方法
Characterized by the heart’s damaged capacity to pump blood effectively, HF arises from a sequence of compromised mechanisms, including mitochondrial dysfunction, imbalance in oxidative metabolism, and prolonged inflammatory reaction, which collectively drive cardiomyocyte apoptosis and myocardial transformation [3, 4].；These components, when integrated across the entire physiology, form a dual-purpose nanodelivery vehicle capable of treating the multi-layered pathological landscape of HF.In this study, we developed a novel nanoplatform (PCM-modified M2 macrophage membrane-coated CeO₂ nanozyme loaded with PGAM5 siRNA (P-MM@Ps-CeO₂)) designed to synergistically target mitochondrial dynamics, oxidative stress, and inflammation in HF.；We evaluated the performance of P-MM@Ps-CeO₂ in vitro using LPS-stimulated HL-1 cardiomyocytes to mimic inflammatory and oxidative stress conditions, and in vivo using a DOX-induced HF mouse model to assess cardiac function, mitochondrial integrity, and myocardial remodeling.
核心结论
Characterized by the heart’s damaged capacity to pump blood effectively, HF arises from a sequence of compromised mechanisms, including mitochondrial dysfunction, imbalance in oxidative metabolism, and prolonged inflammatory reaction, which collectively drive cardiomyocyte apoptosis and myocardial transformation [3, 4].；Functionalized nanoparticles (MM@CeO2 and P-MM@Ps-CeO2) preserved this crystalline form, demonstrating stability during surface modification.；(B) FTIR spectra of CeO₂, HMIM, and Ce(NO₃)₃ confirming successful surface functionalization (C) TEM mapping of P-MM@Ps-CeO₂, demonstrating the uniform distribution of Ce, O, C, and N elements.
局限
Biomimetic coatings, such as M2 macrophage membranes, leverage the anti-inflammatory properties of M2 macrophages and their chemotactic dependence in inflamed tissues, warranting greater attention to delivery and immune modulation [15, 16].；These profiles warrant effective siRNA delivery and ROS scavenging, which are fundamental for HF clinical intervention.；The presence of 7 genes in persistent decline highlights the limitations of current therapy, while the rescue of 154 genes underscores the significant metabolic benefits of PMPC treatment.Fig. 12Comprehensive kinetic profiling and functional landscape of the mitochondrial transcriptome modulated by P-MM@Ps-CeO2.
对本项目的价值
中高价值：属「线粒体质量控制与氧化应激」方向；线粒体功能与氧化应激栏目可用作本项目文献库与综述素材。 ｜ 价值分 3.0/5（★★★☆☆）
全文来源
PubMed PMC JATS（正文 76,794 字符，题名指纹 0.92，已过 PubMed PMCID 官方关联 + 题名指纹 + 正文长度归属校验）
原文题录
- 中文题名：靶向线粒体动力学与氧化应激治疗心力衰竭的多功能仿生纳米平台
- 英文标题：A multifunctional biomimetic nanoplatform targeting mitochondrial dynamics and oxidative stress for heart failure therapy.
- 期刊与标识：Journal of nanobiotechnology · PMID 42968159 · DOI 10.1186/s12951-026-04839-8 · PMC PMC13726084