Authors
Jun Li, Zheng-Long Zhong, Jing Tang, Yi Chen, Chang-Pei Xiang, Jing Li, Ju-Long Tian, Xiao-Ming Luo, Jian-Jie Zou, Yu-Qing Tian
Published in
Journal of translational medicine. Jul 18, 2026. Epub Jul 18, 2026.
Abstract
DOX, an anthracycline antibiotic, is extensively utilized in the treatment of various solid tumors and hematological malignancies but is constrained by its cumulative cardiotoxicity. PDA has emerged as a promising drug delivery platform owing to its superior biocompatibility, pH-responsive drug release capability, and multifunctional surface properties.The FH peptide, which specifically targets Tenascin-C overexpressed in DOX-injured myocardium, offers a promising strategy to enhance cardiac-specific drug accumulation.
In vitro experiments were performed using primary neonatal mouse cardiomyocytes. Cardioprotective efficacy was evaluated in an acute DOX-induced myocardial injury mouse model, and antitumor activity was assessed in a 4T1 tumor-bearing mouse model.
Our comprehensive analysis, including spectroscopic methods and physicochemical characterization, confirmed the successful integration of Dex and FH onto the PDA platform. Both in vitro and in vivo studies demonstrated that PDA-Dex/FH effectively treats DOX-induced cardiotoxicity, with FH incorporation enhancing cardiac targeting while preserving DOX's antitumor efficacy.
we demonstrated that, under the experimental conditions of this study, PDA-Dex/FH not only markedly mitigates myocardial injury with enhanced cardiac accumulation but also retains the chemotherapeutic efficacy of doxorubicin, thereby.
PMID:
42471703
Bibliographic data and abstract were imported from PubMed on 19 Jul 2026.
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