ArticleNature communications2021
Analysing the mechanism of mitochondrial oxidation-induced cell death using a multifunctional iridium(III) photosensitiser.
Article in Nature communications, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 73 citations in OpenAlex.
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- Advances in Coumarin Fluorescent Probes for Medical Diagnostics: A Review of Recent Developments.Biosensors · 2026Review
- Engineered nanomedicine triggering ROS storms for enhanced cancer therapeutics.Regenerative biomaterials · 2026Review
- Targeting myeloid differentiation protein 2 ameliorates rheumatoid arthritis by inhibiting inflammation and ferroptosis via MAPK and NF-κB signaling pathways.Journal of molecular medicine (Berlin, Germany) · 2025Article
- Advancing Multicolor Super-Resolution Volume Imaging: Illuminating Complex Cellular Dynamics.JACS Au · 2025Review
- Fto-dependent Vdac3 m6A Modification Regulates Neuronal Ferroptosis Induced by the Post-ICH Mass Effect and Transferrin.Neuroscience bulletin · 2025Article
- Initial stage of crusted scabies and possible diagnostic characteristics: A case series.Parasitology · 2025Review
- Oxidative cell death in the central nervous system: mechanisms and therapeutic strategies.Frontiers in cell and developmental biology · 2025Review
- Rational Design of Biocompatible Ir(III) Photosensitizer to Overcome Drug-Resistant Cancer via Oxidative Autophagy Inhibition.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Leveraging the Photofunctions of Transition Metal Complexes for the Design of Innovative Phototherapeutics.Small methods · 2024Review
- Enhanced ROS Production and Mitochondrial Metabolic Shifts in CD4International journal of molecular sciences · 2024Article
- Protective Effects ofJournal of pharmacopuncture · 2024Article
- GPCR-Gα13 Involvement in Mitochondrial Function, Oxidative Stress, and Prostate Cancer.International journal of molecular sciences · 2024Review
- Oxidative photocatalysis on membranes triggers non-canonical pyroptosis.Nature communications · 2024Article
- Novel Ultrastructural Insights into the Clear-Cell Carcinoma of the Pancreas: A Case Report.International journal of molecular sciences · 2024Article
- Metallopolymer strategy to explore hypoxic active narrow-bandgap photosensitizers for effective cancer photodynamic therapy.Nature communications · 2024Article
- Interrogating bioinspired ESIPT/PCET-based Ir(iii)-complexes as organelle-targeted phototherapeutics: a redox-catalysis under hypoxia to evoke synergistic ferroptosis/apoptosis.Chemical science · 2023Article
- Mitochondrial DNA-targeted therapy: A novel approach to combat cancer.Cell insight · 2023Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mitochondrial oxidation-induced cell death, a physiological process triggered by various cancer therapeutics to induce oxidative stress on tumours, has been challenging to investigate owing to the difficulties in generating mitochondria-specific oxidative stress and monitoring mitochondrial responses simultaneously. Accordingly, to the best of our knowledge, the relationship between mitochondrial protein oxidation via oxidative stress and the subsequent cell death-related biological phenomena has not been defined. Here, we developed a multifunctional iridium(III) photosensitiser, Ir-OA, capable of inducing substantial mitochondrial oxidative stress and monitoring the corresponding change in viscosity, polarity, and morphology. Photoactivation of Ir-OA triggers chemical modifications in mitochondrial protein-crosslinking and oxidation (i.e., oxidative phosphorylation complexes and channel and translocase proteins), leading to microenvironment changes, such as increased microviscosity and depolarisation. These changes are strongly related to cell death by inducing mitochondrial swelling with excessive fission and fusion. We suggest a potential mechanism from mitochondrial oxidative stress to cell death based on proteomic analyses and phenomenological observations.
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