ReviewAntioxidants & redox signaling2012
Mitochondrial thiols in the regulation of cell death pathways.
Review in Antioxidants & redox signaling, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
57 citing papers in PubMed, 122 citations in OpenAlex.
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- The Switching of the Type of a ROS Signal from Mitochondria: The Role of Respiratory Substrates and Permeability Transition.Antioxidants (Basel, Switzerland) · 2024Article
- Methionine sulfoxide reductase B2 protects against cardiac complications in diabetes mellitus.Diabetology & metabolic syndrome · 2024Article
- Antiproliferative, antimigratory, and apoptotic effects of diffractaic and vulpinic acids as thioredoxin reductase 1 inhibitors on cervical cancer.Naunyn-Schmiedeberg's archives of pharmacology · 2024Article
- The mitochondrial calcium uniporter (MCU) activates mitochondrial respiration and enhances mobility by regulating mitochondrial redox state.Redox biology · 2023Article
- Aquaporin 1 Facilitates Ferroptosis, M1 Polarization, Mitochondrial Dysfunction, and Autophagy Damage on Lipopolysaccharide-Induced Macrophage Through Down-Regulation of P53 Signaling Pathway.DNA and cell biology · 2023Article
- Mitochondrial Transfer as a Novel Therapeutic Approach in Disease Diagnosis and Treatment.International journal of molecular sciences · 2023Review
- Lipid metabolism and Alzheimer's disease: clinical evidence, mechanistic link and therapeutic promise.The FEBS journal · 2023Review
- Glutathione-Related Enzymes and Proteins: A Review.Molecules (Basel, Switzerland) · 2023Review
- NAC, NAC, Knockin' on Heaven's door: Interpreting the mechanism of action of N-acetylcysteine in tumor and immune cells.Redox biology · 2022Review
- TIGAR alleviates oxidative stress in brain with extended ischemia via a pentose phosphate pathway-independent manner.Redox biology · 2022Article
- Determination of low molecular thiols and protein sulfhydryl groups using heterocyclic disulfides.Amino acids · 2022Article
- The Link between Oxidative Stress, Redox Status, Bioenergetics and Mitochondria in the Pathophysiology of ALS.International journal of molecular sciences · 2021Review
- Molecular and Supramolecular Structure of the Mitochondrial Oxidative Phosphorylation System: Implications for Pathology.Life (Basel, Switzerland) · 2021Review
- Changes in Glutathione Content in Liver Diseases: An Update.Antioxidants (Basel, Switzerland) · 2021Review
- Selenium Deficiency in Chickens Induces Intestinal Mucosal Injury by Affecting the Mucosa Morphology, SIgA Secretion, and GSH-Px Activity.Biological trace element research · 2020Article
- Mitochondrial Glutathione: Recent Insights and Role in Disease.Antioxidants (Basel, Switzerland) · 2020Review
- Redox basis of exercise physiology.Redox biology · 2020Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
significanceRegulation of mitochondrial H(2)O(2) homeostasis and its involvement in the regulation of redox-sensitive signaling and transcriptional pathways is the consequence of the concerted activities of the mitochondrial energy- and redox systems. RECENT ADVANCES: The energy component of this mitochondrial energy-redox axis entails the formation of reducing equivalents and their flow through the respiratory chain with the consequent electron leak to generate [Formula: see text] and H(2)O(2). The mitochondrial redox component entails the thiol-based antioxidant system, largely accounted for by glutathione- and thioredoxin-based systems that support the activities of glutathione peroxidases, peroxiredoxins, and methionine sulfoxide reductase. The ultimate reductant for these systems is NADPH: mitochondrial sources of NADPH are the nicotinamide nucleotide transhydrogenase, isocitrate dehydrogenase-2, and malic enzyme. NADPH also supports the glutaredoxin activity that regulates the extent of S-glutathionylation of mitochondrial proteins in response to altered redox status. CRITICAL ISSUES: The integrated network of these mitochondrial thiols constitute a regulatory device involved in the maintenance of steady-state levels of H(2)O(2), mitochondrial and cellular redox and metabolic homeostasis, as well as the modulation of cytosolic redox-sensitive signaling; disturbances of this regulatory device affects transcription, growth, and ultimately influences cell survival/death. FUTURE DIRECTIONS: The modulation of key mitochondrial thiol proteins, which participate in redox signaling, maintenance of the bioenergetic machinery, oxidative stress responses, and cell death programming, provides a pivotal direction in developing new therapies towards the prevention and treatment of several diseases.
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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.