ArticleNature communications2024
Mitochondrial respiratory function is preserved under cysteine starvation via glutathione catabolism in NSCLC.
Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
24 citing papers in PubMed.
- Triple-Microenvironment Decoding Enables Logic-Unlocked Precision Photoimmunotherapy.Angewandte Chemie (International ed. in English) · 2026Article
- A targetable FTO/SLC7A11/CBS/CTH axis controls cysteine metabolism, growth and survival in NSCLC.Science advances · 2026Article
- Glucose starvation induces fumarate hydratase succinylation and inhibits ferroptosis to maintain colon cancer cell proliferation.Cell death & disease · 2026Article
- Article
- Coenzyme A mitigates cystine-deprivation-induced ferroptosis by suppressing the iron-starvation response.The FEBS journal · 2026Article
- hUCMSC-exosomes attenuate acute lung injury by inhibiting ferroptosis in pulmonary microvascular endothelial cells through ribosomal protein RPS11 upregulation.Journal of nanobiotechnology · 2026Article
- Article
- Comparative analysis of naked mole-rat thermogenesis and its potential to maintain euthermia in response to cold.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Dissecting Complex Interactions Between Ferroptosis and the Proteasome.bioRxiv : the preprint server for biology · 2026Article
- Life Cells for future energy systems: adaptation, evolution and exploration.National science review · 2026Review
- BACH1-CHAC1-Glutathione Axis Aggravates Myocardial Ischemia-Reperfusion Injury by Enhancing Ferroptosis and Oxidative Stress.Antioxidants (Basel, Switzerland) · 2026Article
- Distinct control of T cell proliferation and effector function by partitioning of intracellular sulfur from cysteine.bioRxiv : the preprint server for biology · 2026Article
- Long Non-Coding RNA PVT1 Promotes Doxorubicin Resistance by Inhibiting Ferroptosis in Breast Cancer.Breast cancer (Dove Medical Press) · 2026Article
- Best practices for cysteine analysis.Ferroptosis and oxidative stress · 2026Article
- NDUFA8 promotes cell viability and inhibits ferroptosis and cisplatin sensitivity by stabilizing Fe-S clusters in cervical cancer.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- Aberrant Mitochondrial Metabolism in Alzheimer's Disease Links Energy Stress with Ferroptosis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- From mitochondrial dysregulation to ferroptosis: Exploring new strategies and challenges in radioimmunotherapy (Review).International journal of oncology · 2025Review
- Thioredoxin Reductase 1 inhibition triggers ferroptosis in KRAS-independent lung cancers.bioRxiv : the preprint server for biology · 2025Article
- Increased antioxidative defense and reduced advanced glycation end-product formation by metabolic adaptation in non-small-cell-lung-cancer patients.Nature communications · 2025Article
- The strategic breakdown: CHAC enzymes as regulators of glutathione homeostasis and disease implications.Frontiers in molecular biosciences · 2025Review
Corrections and comments
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Authors and funding
7 authors.
Funding
Abstract
Cysteine metabolism occurs across cellular compartments to support diverse biological functions and prevent the induction of ferroptosis. Though the disruption of cytosolic cysteine metabolism is implicated in this form of cell death, it is unknown whether the substantial cysteine metabolism resident within the mitochondria is similarly pertinent to ferroptosis. Here, we show that despite the rapid depletion of intracellular cysteine upon loss of extracellular cystine, cysteine-dependent synthesis of Fe-S clusters persists in the mitochondria of lung cancer cells. This promotes a retention of respiratory function and a maintenance of the mitochondrial redox state. Under these limiting conditions, we find that glutathione catabolism by CHAC1 supports the mitochondrial cysteine pool to sustain the function of the Fe-S proteins critical to oxidative metabolism. We find that disrupting Fe-S cluster synthesis under cysteine restriction protects against the induction of ferroptosis, suggesting that the preservation of mitochondrial function is antagonistic to survival under starved conditions. Overall, our findings implicate mitochondrial cysteine metabolism in the induction of ferroptosis and reveal a mechanism of mitochondrial resilience in response to nutrient stress.
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