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Peer-reviewedCC BYMaterials Today Bio

Targeted delivery of celastrol and siRNA via macrophage biomimetic nanoparticles for doxorubicin-induced cardiomyopathy therapy

  • Qiyu Zhang1
  • Tianyu Guo2
  • Xuna Xue2
  • Zhibo Zhang2
  • Xinyan Liu2
  • Qing Cai2
  • Ning Wang3
  • Bo Zhang4
  • Jinyong Peng5
5 affiliations
  1. 1Institute of Integrative Medicine, Dalian Medical University, Western 9 Lvshunnan Road, Dalian, 116044, China; College of Pharmacy, Dalian Medical University, Western 9 Lvshunnan Road, Dalian, 116044, China
  2. 2College of Pharmacy, Dalian Medical University, Western 9 Lvshunnan Road, Dalian, 116044, China
  3. 3College of Pharmacy, Dalian Medical University, Western 9 Lvshunnan Road, Dalian, 116044, China; Corresponding author. College of Pharmacy, Dalian Medical University, Dalian, 116044, China.
  4. 4Department of Cardiology, First Affiliated Hospital of Dalian Medical University, Dalian, 116044, China; Corresponding author.Department of Cardiology, First Affiliated Hospital of Dalian Medical University, Dalian, 116044, China.
  5. 5College of Pharmacy, Dalian Medical University, Western 9 Lvshunnan Road, Dalian, 116044, China; College of Pharmacy, Hubei Shizhen Laboratory, Hubei University of Chinese Medicine, Wuhan, 430065, China; Corresponding author. College of Pharmacy, Dalian Medical University, Dalian, 116044, China.
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Abstract

Doxorubicin-induced cardiomyopathy (DIC) is a severe complication following anthracycline chemotherapy, and its main pathogenesis is inflammatory responses and ferroptosis. This study constructed hyaluronic acid-based macrophage biomimetic nanoparticles (M@HCDA) to co-delivery of Celastrol (Cel) and siADAM17 for the treatment of DIC. This research revealed that Cel exerted an anti-ferroptosis effect by regulating GPX4 and SLC7A11, while siADAM17 inhibited TAK1-MAPK pathway activation by silencing ADAM17. Meanwhile, the synergistic effect of Cel and siADAM17 significantly alleviated oxidative stress, myocardial fibrosis, apoptosis, and mitochondrial dysfunction, thereby relieving myocardial injury caused by DOX-induced cardiotoxicity and providing effective early cardioprotection. In vitro and in vivo experiments indicated that M@HCDA exhibited good stability, biocompatibility, and targeting capability, showing the clinical application potential. The design and development of M@HCDA provide new experimental evidence and candidate strategy for treating DIC.

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Cite

BibTeXRIS
BibTeX
@article{zhang2026targeted,
  title = {{Targeted delivery of celastrol and siRNA via macrophage biomimetic nanoparticles for doxorubicin-induced cardiomyopathy therapy}},
  author = {Qiyu Zhang and Tianyu Guo and Xuna Xue and Zhibo Zhang and Xinyan Liu and Qing Cai and Ning Wang and Bo Zhang and Jinyong Peng},
  journal = {Materials Today Bio},
  year = {2026},
  month = oct,
  doi = {10.1016/j.mtbio.2026.103779},
  url = {https://doi.org/10.1016/j.mtbio.2026.103779},
  note = {CC BY},
}
RIS
TY  - JOUR
TI  - Targeted delivery of celastrol and siRNA via macrophage biomimetic nanoparticles for doxorubicin-induced cardiomyopathy therapy
AU  - Qiyu Zhang
AU  - Tianyu Guo
AU  - Xuna Xue
AU  - Zhibo Zhang
AU  - Xinyan Liu
AU  - Qing Cai
AU  - Ning Wang
AU  - Bo Zhang
AU  - Jinyong Peng
PY  - 2026
DA  - 2026/10/23
JO  - Materials Today Bio
DO  - 10.1016/j.mtbio.2026.103779
UR  - https://doi.org/10.1016/j.mtbio.2026.103779
AB  - Doxorubicin-induced cardiomyopathy (DIC) is a severe complication following anthracycline chemotherapy, and its main pathogenesis is inflammatory responses and ferroptosis. This study constructed hyaluronic acid-based macrophage biomimetic nanoparticles (M@HCDA) to co-delivery of Celastrol (Cel) and siADAM17 for the treatment of DIC. This research revealed that Cel exerted an anti-ferroptosis effect by regulating GPX4 and SLC7A11, while siADAM17 inhibited TAK1-MAPK pathway activation by silencing ADAM17. Meanwhile, the synergistic effect of Cel and siADAM17 significantly alleviated oxidative stress, myocardial fibrosis, apoptosis, and mitochondrial dysfunction, thereby relieving myocardial injury caused by DOX-induced cardiotoxicity and providing effective early cardioprotection. In vitro and in vivo experiments indicated that M@HCDA exhibited good stability, biocompatibility, and targeting capability, showing the clinical application potential. The design and development of M@HCDA provide new experimental evidence and candidate strategy for treating DIC.
SN  - 2590-0064
ER  -