Engineering a bi-functional nanoplatform containing FH peptide for preferential cardiac delivery to counteract doxorubicin-induced cardiotoxicity
- 1Hospital of Traditional Chinese Medicine and Western Medicine of Panzhihua
Abstract
Background 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. Methods 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. Results 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. Conclusions 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.
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BibTeX
@article{li2026engineering,
title = {{Engineering a bi-functional nanoplatform containing FH peptide for preferential cardiac delivery to counteract doxorubicin-induced cardiotoxicity}},
author = {Jun Li and Zheng-long Zhong and Jing Tang and Yi Chen and Chang-pei Xiang and Jing Li and Ju-long Tian and Xiao-ming Luo and Jian-jie Zou and Yu-qing Tian},
journal = {Journal of Translational Medicine},
year = {2026},
month = jul,
doi = {10.1186/s12967-026-08617-w},
url = {https://doi.org/10.1186/s12967-026-08617-w},
note = {CC BY},
}
RIS
TY - JOUR
TI - Engineering a bi-functional nanoplatform containing FH peptide for preferential cardiac delivery to counteract doxorubicin-induced cardiotoxicity
AU - Jun Li
AU - Zheng-long Zhong
AU - Jing Tang
AU - Yi Chen
AU - Chang-pei Xiang
AU - Jing Li
AU - Ju-long Tian
AU - Xiao-ming Luo
AU - Jian-jie Zou
AU - Yu-qing Tian
PY - 2026
DA - 2026/07/01
JO - Journal of Translational Medicine
DO - 10.1186/s12967-026-08617-w
UR - https://doi.org/10.1186/s12967-026-08617-w
AB - Background 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. Methods 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. Results 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. Conclusions 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.
SN - 1479-5876
ER -