ReviewRedox report : communications in free radical research2015
Sepsis, oxidative stress, and hypoxia: Are there clues to better treatment?
Review in Redox report : communications in free radical research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
43 citing papers in PubMed, 85 citations in OpenAlex.
- Oxidation Reduction Potential (ORP) is Predictive of Complications Following Pediatric Cardiac Surgery.Pediatric cardiology · 2018Trial
- Increased static and decreased capacity oxidation-reduction potentials in plasma are predictive of metabolic syndrome.Redox biology · 2017Trial
- The role of α-hydroxybutyrate in modulating sepsis progression: identification of key targets and biomarkers through multi-database data mining, machine learning, and unsupervised clustering.Frontiers in pharmacology · 2025Article
- Decoding Sepsis: Unraveling Key Signaling Pathways for Targeted Therapies.Research (Washington, D.C.) · 2025Review
- Adaptation of Natural Killer Cells to Hypoxia: A Review of the Transcriptional, Translational, and Metabolic Processes.ImmunoTargets and therapy · 2025Review
- Machine learning for predicting acute myocardial infarction in patients with sepsis.Scientific reports · 2024Article
- Neohesperidin Dihydrochalcone Alleviates Lipopolysaccharide-Induced Vascular Endothelium Dysfunction by Regulating Antioxidant Capacity.Immunity, inflammation and disease · 2024Article
- Oxidative/Nitrosative Stress and Brain Involvement in Sepsis: A Relationship Supported by Immunohistochemistry.Medicina (Kaunas, Lithuania) · 2024Article
- Treatment of Acute and Long-COVID, Diabetes, Myocardial Infarction, and Alzheimer's Disease: The Potential Role of a Novel Nano-Compound-The Transdermal Glutathione-Cyclodextrin Complex.Antioxidants (Basel, Switzerland) · 2024Review
- From Molecular Mechanisms to Clinical Therapy: Understanding Sepsis-Induced Multiple Organ Dysfunction.International journal of molecular sciences · 2024Review
- Review
- Plasma Ascorbic Acid Levels in Critically Ill Pediatric Patients.Journal of pediatric intensive care · 2024Article
- CD5L as a promising biological therapeutic for treating sepsis.Nature communications · 2024Article
- Bisphosphoglycerate mutase predicts myocardial dysfunction and adverse outcome in sepsis: an observational cohort study.BMC infectious diseases · 2024Observational
- Mechanisms underlying delirium in patients with critical illness.Frontiers in aging neuroscience · 2024Review
- Inflammatory mechanisms and intervention strategies for sepsis-induced myocardial dysfunction.Immunity, inflammation and disease · 2023Review
- Aldehyde Dehydrogenase 2 Ameliorates LPS-Induced Acute Kidney Injury through Detoxification of 4-HNE and Suppression of the MAPK Pathway.Journal of immunology research · 2023Article
- Small molecule inhibiting microglial nitric oxide release could become a potential treatment for neuroinflammation.PloS one · 2023Article
- Low dimensional nanomaterials for treating acute kidney injury.Journal of nanobiotechnology · 2022Review
- Oxygen therapy for sepsis and prevention of complications.Acute and critical care · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Sepsis is a clinical syndrome characterized by systemic inflammation, usually in response to infection. The signs and symptoms are very similar to Systemic Inflammatory Response Syndrome (SIRS), which typically occur consequent to trauma and auto-immune diseases. Common treatments of sepsis include administration of antibiotics and oxygen. Oxygen is administered due to ischemia in tissues, which results in the production of free radicals. Poor utilization of oxygen by the mitochondrial electron transport chain can increase oxidative stress during ischemia and exacerbate the severity and outcome in septic patients. This course of treatment virtually mimics the conditions seen in ischemia-reperfusion disorders. Therefore, this review proposes that the mechanism of free radical production seen in sepsis and SIRS is identical to the oxidative stress seen in ischemia-reperfusion injury. Specifically, this is due to a biochemical mechanism within the mitochondria where the oxidation of succinate to fumarate by succinate dehydrogenase (complex II) is reversed in sepsis (hypoxia), leading to succinate accumulation. Oxygen administration (equivalent to reperfusion) rapidly oxidizes the accumulated succinate, leading to the generation of large amounts of superoxide radical and other free radical species. Organ damage possibly leading to multi-organ failure could result from this oxidative burst seen in sepsis and SIRS. Accordingly, we postulate that temporal administration with anti-oxidants targeting the mitochondria and/or succinate dehydrogenase inhibitors could be beneficial in sepsis and SIRS patients.
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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.