ArticleCell chemical biology2019
Selective Disruption of Mitochondrial Thiol Redox State in Cells and In Vivo.
Article in Cell chemical biology, 2019. 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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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.
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Who cites it
28 citing papers in PubMed, 53 citations in OpenAlex.
- Dual-action mitochondria-targeted prodrugs that both deplete mitochondrial glutathione and deliver a toxic payload to the matrix.European journal of medicinal chemistry · 2026Article
- Glutathione responsive nanomedicine leverages tumor redox imbalance for targeted cancer theranostics.Discover oncology · 2026Review
- Mitochondrial glutathione transporter SLC25A40 regulates macrophage cytokine production.Scientific reports · 2025Article
- The human zinc-binding cysteine proteome.Cell · 2025Article
- Human mitochondrial glutathione transferases: Kinetic parameters and accommodation of a mitochondria-targeting group in substrates.Bioorganic & medicinal chemistry · 2024Article
- Functional-metabolic coupling in distinct renal cell types coordinates organ-wide physiology and delays premature ageing.Nature communications · 2023Article
- Optineurin tunes outside-in signaling to regulate lysosome biogenesis and phagocytic clearance in the retina.Current biology : CB · 2023Article
- Glutathionylation of pyruvate dehydrogenase complex E2 and inflammatory cytokine production during acute inflammation are magnified by mitochondrial oxidative stress.Redox biology · 2023Article
- Incorporating a Polyethyleneglycol Linker to Enhance the Hydrophilicity of Mitochondria-Targeted Triphenylphosphonium Constructs.Chembiochem : a European journal of chemical biology · 2023Article
- Mitochondrial transplantation: opportunities and challenges in the treatment of obesity, diabetes, and nonalcoholic fatty liver disease.Journal of translational medicine · 2022Review
- Mitochondrial outer membrane protein FUNDC2 promotes ferroptosis and contributes to doxorubicin-induced cardiomyopathy.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Synthesis of a fluorinated pyronin that enables blue light to rapidly depolarize mitochondria.RSC medicinal chemistry · 2022Article
- Unique assembly of carbonylpyridinium and chromene reveals mitochondrial thiol starvation under ferroptosis and novel ferroptosis inducer.Chemical science · 2022Article
- Ester Prodrugs of Malonate with Enhanced Intracellular Delivery Protect Against Cardiac Ischemia-Reperfusion Injury In Vivo.Cardiovascular drugs and therapy · 2022Article
- Disruption of the TCA cycle reveals an ATF4-dependent integration of redox and amino acid metabolism.eLife · 2021Article
- Article
- Thioredoxin-1 Rescues MPPMolecular neurobiology · 2021Article
- Mechanism of succinate efflux upon reperfusion of the ischaemic heart.Cardiovascular research · 2021Article
- Insights on Targeting Small Molecules to the Mitochondrial Matrix and the Preparation of MitoB and MitoP as Exomarkers of Mitochondrial Hydrogen Peroxide.Methods in molecular biology (Clifton, N.J.) · 2021Article
- On the mechanisms underlying attenuated redox responses to exercise in older individuals: A hypothesis.Free radical biology & medicine · 2020Article
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Authors and funding
20 authors at 3 institutions in 1 country.
Funding
Abstract
Mitochondrial glutathione (GSH) and thioredoxin (Trx) systems function independently of the rest of the cell. While maintenance of mitochondrial thiol redox state is thought vital for cell survival, this was not testable due to the difficulty of manipulating the organelle's thiol systems independently of those in other cell compartments. To overcome this constraint we modified the glutathione S-transferase substrate and Trx reductase (TrxR) inhibitor, 1-chloro-2,4-dinitrobenzene (CDNB) by conjugation to the mitochondria-targeting triphenylphosphonium cation. The result, MitoCDNB, is taken up by mitochondria where it selectively depletes the mitochondrial GSH pool, catalyzed by glutathione S-transferases, and directly inhibits mitochondrial TrxR2 and peroxiredoxin 3, a peroxidase. Importantly, MitoCDNB inactivates mitochondrial thiol redox homeostasis in isolated cells and in vivo, without affecting that of the cytosol. Consequently, MitoCDNB enables assessment of the biomedical importance of mitochondrial thiol homeostasis in reactive oxygen species production, organelle dynamics, redox signaling, and cell death in cells and in vivo.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.