Recent Advances in Mitochondria-Targeted Nanoparticle Photodynamic Therapy for Triple-Negative Breast Cancer
- 1Doctoral School, Medical College of the University of Rzeszów, 35-310 Rzeszów, Poland
- 2Department of Biochemistry and General Chemistry, Medical College of the University of Rzeszów, 35-310 Rzeszów, Poland
Abstract
Triple-negative breast cancer (TNBC) remains a therapeutically challenging and biologically heterogeneous breast cancer subtype, prompting the development of strategies that exploit specific subcellular vulnerabilities. Mitochondria represent an attractive target for photodynamic therapy (PDT) because the short lifetime and limited diffusion range of photogenerated reactive oxygen species make their site of generation a critical determinant of cellular damage. This review critically examines recent nanoparticle-based approaches to mitochondria-targeted PDT in TNBC, with particular emphasis on nanoplatform design, experimental evidence for mitochondrial localisation, amplification of mitochondrial oxidative stress, regulated cell-death pathways, and preclinical efficacy. A structured search of PubMed, Scopus, and Web of Science identified 3637 records, of which seven original studies ultimately fulfilled the predefined criteria for nanoparticle-mediated classical PDT in TNBC with mitochondrial targeting. The analysed platforms employed intrinsic mitochondrial affinity of photosensitisers, mitochondriotropic ligands, and multistage delivery strategies, while therapeutic amplification involved type I photochemistry, modulation of oxygen availability and consumption, glutathione depletion, metabolic interference, plasmonic enhancement, and combined PDT/PTT. Mitochondrial photodamage was associated with apoptosis, pyroptosis, immunogenic cell death, cGAS–STING signalling, and antitumour immune activation. Despite encouraging preclinical results, the evidence remains limited by the small number of studies, dominance of 4T1-based models, variable strength of mitochondrial-targeting validation, and limited translational assessment. Future development should focus on mechanistically validated targeting, clinically representative TNBC models, simplified nanoplatform design, and demonstration of a clear therapeutic advantage over less complex PDT systems.
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BibTeX
@article{przygorzewska2026recent,
title = {{Recent Advances in Mitochondria-Targeted Nanoparticle Photodynamic Therapy for Triple-Negative Breast Cancer}},
author = {Agnieszka Przygórzewska and Dorota Bartusik-Aebisher},
journal = {International Journal of Molecular Sciences},
year = {2026},
month = nov,
doi = {10.3390/ijms27219975},
url = {https://www.mdpi.com/1422-0067/27/21/9975},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - Recent Advances in Mitochondria-Targeted Nanoparticle Photodynamic Therapy for Triple-Negative Breast Cancer
AU - Agnieszka Przygórzewska
AU - Dorota Bartusik-Aebisher
PY - 2026
DA - 2026/11/07
JO - International Journal of Molecular Sciences
DO - 10.3390/ijms27219975
UR - https://www.mdpi.com/1422-0067/27/21/9975
AB - Triple-negative breast cancer (TNBC) remains a therapeutically challenging and biologically heterogeneous breast cancer subtype, prompting the development of strategies that exploit specific subcellular vulnerabilities. Mitochondria represent an attractive target for photodynamic therapy (PDT) because the short lifetime and limited diffusion range of photogenerated reactive oxygen species make their site of generation a critical determinant of cellular damage. This review critically examines recent nanoparticle-based approaches to mitochondria-targeted PDT in TNBC, with particular emphasis on nanoplatform design, experimental evidence for mitochondrial localisation, amplification of mitochondrial oxidative stress, regulated cell-death pathways, and preclinical efficacy. A structured search of PubMed, Scopus, and Web of Science identified 3637 records, of which seven original studies ultimately fulfilled the predefined criteria for nanoparticle-mediated classical PDT in TNBC with mitochondrial targeting. The analysed platforms employed intrinsic mitochondrial affinity of photosensitisers, mitochondriotropic ligands, and multistage delivery strategies, while therapeutic amplification involved type I photochemistry, modulation of oxygen availability and consumption, glutathione depletion, metabolic interference, plasmonic enhancement, and combined PDT/PTT. Mitochondrial photodamage was associated with apoptosis, pyroptosis, immunogenic cell death, cGAS–STING signalling, and antitumour immune activation. Despite encouraging preclinical results, the evidence remains limited by the small number of studies, dominance of 4T1-based models, variable strength of mitochondrial-targeting validation, and limited translational assessment. Future development should focus on mechanistically validated targeting, clinically representative TNBC models, simplified nanoplatform design, and demonstration of a clear therapeutic advantage over less complex PDT systems.
SN - 1422-0067
ER -