ArticleAntioxidants (Basel, Switzerland)2025
Cytochrome c Oxidase Subunit COX4-1 Reprograms Erastin-Induced Cell Death from Ferroptosis to Apoptosis: A Transmitochondrial Study.
Article in Antioxidants (Basel, Switzerland), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Mitochondrial dysfunction and the regulatory cell death crosstalk network in chronic obstructive pulmonary disease: from oxidative stress mechanisms to targeted therapeutic strategies.Frontiers in immunology · 2026Review
- From gut-reproductive microbiota to ferroptosis: a comprehensive insight into the molecular-pathogenicity of endometriosis.Frontiers in immunology · 2026Review
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Authors and funding
3 authors.
Funding
Abstract
Ferroptosis is an iron-dependent, oxidative form of regulated cell death that has emerged as a therapeutic vulnerability in glioblastoma; however, the mitochondrial determinants that govern ferroptotic sensitivity remain poorly defined. Cytochrome c oxidase (CcO/Complex IV), a key regulator of mitochondrial respiration, contains two isoforms of subunit IV (COX4): COX4-1, a housekeeping isoform, and COX4-2, a stress-inducible variant. We previously found that COX4-1 expression protects glioma cells from erastin-induced ferroptosis, suggesting that mitochondria influence cell-death decisions independently of canonical ferroptotic regulators. Here, we used CRISPR-generated POLG-knockout ρ
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