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[] Severe prolonged oxidative damage can lower glutathione levels by increased production and collection of glutathione disulphide, outflow and plasma breakdown, peptide S-glutathionylation and the formation of glutathione compounds

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Ophthalmologic examinations, such as retinal OCT-A or autofluorescence tests, do not specifically detect ferroptosis and are difficult to use for efficacy monitoring and patient stratification

Collectively, this dual metabolic identity, preserving physiological specialization in citrate production while hijacking polyamine and citrate pathways for oncogenic rewiring, not only distinguishes PCa from other malignancies but also unveils targetable vulnerabilities for diagnostic and therapeutic innovation

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Long noncoding RNA as modular scaffold of histone modification complexes