Skip to content
DraconiticResearch
Search Sources API
203,234 studies31 sourcesUpdated 24 min ago
Peer-reviewedCC BYNano-Micro Letters

Advances in Polydopamine-Based Nanoplatforms: Antioxidant Mechanisms and Applications in Oxidative Stress-Mediated Diseases

6 affiliations
  1. 1Department of Pharmaceutics, School of Pharmacy, Shenyang Pharmaceutical University, Shenyang, 110016, People's Republic of China
  2. 2Department of Microbial and Biochemical Pharmacy, School of Life Sciences and Biopharmaceuticals, Shenyang Pharmaceutical University, Shenyang, 110016, People's Republic of China
  3. 3Department of Ultrasound, Shengjing Hospital of China Medical University, Shenyang, 110004, People's Republic of China. [email protected]
  4. 4Department of Pharmacy, The First Hospital of China Medical University, 155 Nanjing North Street, Shenyang, 110001, People's Republic of China. [email protected]
  5. 5Department of Pharmaceutics, School of Pharmacy, Shenyang Pharmaceutical University, Shenyang, 110016, People's Republic of China. [email protected]
  6. 6Joint International Research Laboratory of Intelligent Drug Delivery Systems, Ministry of Education, Shenyang, 110016, People's Republic of China. [email protected]

Abstract

Polydopamine (PDA) exhibits unique advantages in the treatment of oxidative damage owing to its melanin-mimetic structure, abundant redox-active functional groups, and excellent biocompatibility. Distinct from conventional antioxidant molecules, PDA-based nanoplatforms can efficiently eliminate reactive oxygen species (ROS) via hydrogen atom transfer and electron transfer mechanisms, while relying on the dynamic redox cycling of catechol/quinone moieties to achieve sustained antioxidant activity. However, systematic summaries of PDA-based antioxidant nanoplatforms remain relatively limited. Therefore, this review provides a comprehensive overview of the antioxidant mechanisms of PDA and its associated physicochemical properties, with particular emphasis on the design strategies of diverse PDA-based nanoplatforms, including solid, mesoporous, hollow, doped, and coated architectures, as well as the effects of structural features, particle size, composition, and surface charge on their antioxidant performance. In addition, recent research progress is systematically categorized around core pathological challenges, including breaking ROS-inflammation feedback loops, overcoming biological delivery barriers, remodeling regenerative microenvironments, and regulating programmed cell death.

Related

  1. Polyoxometalate-controlled oxidative formation of bioinspired polydopamine hydrogels
    Paul Kadereit, Marius G. Braun, Martin Diefenbach +4
    ChemRxivPreprintCC BY-NC-NDMaterials & polymersChemRxiv
  2. Tailoring nanoplatforms for depression applications
    Xiaoyan Li, Shilin Wen, Keer Zhang +6
    Journal of Translational MedicinePeer-reviewedCC BY-NC-ND 4.0Full textMaterials & polymersPMC
  3. Coarse‐Grained Molecular Dynamics Simulations of Oxidative Aging and Stabilization in Polymer Melts With Primary Antioxidants: Effects of Antioxidant Concentration and Molecular Architecture
    Takato Ishida, Emmanuel Richaud
    Journal of Vinyl and Additive TechnologyPeer-reviewedCC BY 4.0Full text2 citedMaterials & polymersTheoretical & computational chemistryHAL
  4. Oxidative Stress and Antioxidant Vitamin Profile in Term Neonates with Indirect Hyperbilirubinaemia: A Case–Control Study
    Enas Jabbar Hasan, Abeer J. Hassan, Ammar Adil Jasim
    International Journal of Molecular and Cellular MedicinePeer-reviewedCC BY-NCFull textGenetics & genomicsGeneral chemistryDOAJ
  5. Oleuropein and punicic acid induce oxidative stress and cytotoxicity in MCF-7 breast cancer cells, with protection by peroxiredoxin antioxidant proteins
    Samantha Diiorio, Braden Quitmeyer, Shelley A. Phelan
    Molecular Biology ReportsPeer-reviewedCC BY 4.0Full textOrganic chemistryPMC
BibTeX
@article{wang2026advances,
  title = {{Advances in Polydopamine-Based Nanoplatforms: Antioxidant Mechanisms and Applications in Oxidative Stress-Mediated Diseases}},
  author = {Zhilin Wang and Zhu Liu and Luming Song and Xinyi Zhao and Shuaipeng Feng and Donghua Di and Hao Ju and Long Wan and Qinfu Zhao},
  journal = {Nano-Micro Letters},
  year = {2026},
  month = may,
  doi = {10.1007/s40820-026-02205-9},
  url = {https://doi.org/10.1007/s40820-026-02205-9},
  note = {CC BY},
}
RIS
TY  - JOUR
TI  - Advances in Polydopamine-Based Nanoplatforms: Antioxidant Mechanisms and Applications in Oxidative Stress-Mediated Diseases
AU  - Zhilin Wang
AU  - Zhu Liu
AU  - Luming Song
AU  - Xinyi Zhao
AU  - Shuaipeng Feng
AU  - Donghua Di
AU  - Hao Ju
AU  - Long Wan
AU  - Qinfu Zhao
PY  - 2026
DA  - 2026/05/18
JO  - Nano-Micro Letters
DO  - 10.1007/s40820-026-02205-9
UR  - https://doi.org/10.1007/s40820-026-02205-9
AB  - Polydopamine (PDA) exhibits unique advantages in the treatment of oxidative damage owing to its melanin-mimetic structure, abundant redox-active functional groups, and excellent biocompatibility. Distinct from conventional antioxidant molecules, PDA-based nanoplatforms can efficiently eliminate reactive oxygen species (ROS) via hydrogen atom transfer and electron transfer mechanisms, while relying on the dynamic redox cycling of catechol/quinone moieties to achieve sustained antioxidant activity. However, systematic summaries of PDA-based antioxidant nanoplatforms remain relatively limited. Therefore, this review provides a comprehensive overview of the antioxidant mechanisms of PDA and its associated physicochemical properties, with particular emphasis on the design strategies of diverse PDA-based nanoplatforms, including solid, mesoporous, hollow, doped, and coated architectures, as well as the effects of structural features, particle size, composition, and surface charge on their antioxidant performance. In addition, recent research progress is systematically categorized around core pathological challenges, including breaking ROS-inflammation feedback loops, overcoming biological delivery barriers, remodeling regenerative microenvironments, and regulating programmed cell death.
SN  - 2150-5551
SN  - 2311-6706
ER  -