ReviewNeurochemistry international2017
Targeting antioxidant enzyme expression as a therapeutic strategy for ischemic stroke.
Review in Neurochemistry international, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 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
52 citing papers in PubMed, 109 citations in OpenAlex.
- PI3K-Akt signaling network crosstalk in cerebral ischemia/reperfusion injury: Mechanisms and therapeutic implications.Chinese medical journal · 2026Review
- Serum phosphoproteome alterations associated with cardiac troponin I levels in acute myocardial infarction.Turkish journal of medical sciences · 2026Article
- Targeting Ischemic Stroke with Neural Stem Cells: Insights into Endogenous Repair Mechanisms, Biomaterial-Based Delivery, and Exosome Therapies.Molecular neurobiology · 2025Review
- Therapeutic spectrum of Piperine in ischemic stroke: a literature review.Molecular biology reports · 2025Review
- In Vivo Neuroprotective Effects of Alpinetin Against Experimental Ischemic Stroke Damage Through Antioxidant and Anti-Inflammatory Mechanisms.International journal of molecular sciences · 2025Article
- Nitroxidative Stress, Cell-Signaling Pathways, and Manganese Porphyrins: Therapeutic Potential in Neuropathic Pain.International journal of molecular sciences · 2025Review
- Identification of stroke biomarkers using proteomic profiling of extracellular vesicles derived from human blood: a preliminary study.Frontiers in neurology · 2025Article
- Metallothionein-1A (MT1A) Gene Variability May Play a Role in Female Frailty: A Preliminary Study.Genes · 2024Article
- RNF13 protects neurons against ischemia-reperfusion injury via stabilizing p62-mediated Nrf2/HO-1 signaling pathway.Cell communication and signaling : CCS · 2024Article
- Exploration of SOD3 from gene to therapeutic prospects: a brief review.Molecular biology reports · 2024Review
- Neuroprotective Effects ofNeurochemical research · 2024Article
- Article
- Neuroprotection during Thrombectomy for Acute Ischemic Stroke: A Review of Future Therapies.International journal of molecular sciences · 2024Review
- A Comprehensive Review on the Significance of Cysteine in Various Metabolic Disorders; Particularly CVD, Diabetes, Renal Dysfunction, and Ischemic Stroke.Current protein & peptide science · 2024Review
- Analysis of miRNAs involved in mouse brain injury upon Coxsackievirus A6 infection.Frontiers in cellular and infection microbiology · 2024Article
- Biomimetic nanoparticles in ischemic stroke therapy.Discover nano · 2023Review
- Pyroptosis in neurodegenerative diseases: from bench to bedside.Cell biology and toxicology · 2023Review
- The Impact of Cerebral Ischemia on Antioxidant Enzymes Activity and Neuronal Damage in the Hippocampus.Cellular and molecular neurobiology · 2023Review
- Review
- Aucubin Exerts Neuroprotection against Forebrain Ischemia and Reperfusion Injury in Gerbils through Antioxidative and Neurotrophic Effects.Antioxidants (Basel, Switzerland) · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
During ischemic stroke, neurons and glia are subjected to damage during the acute and neuroinflammatory phases of injury. Production of reactive oxygen species (ROS) from calcium dysregulation in neural cells and the invasion of activated immune cells are responsible for stroke-induced neurodegeneration. Scientists have failed thus far to identify antioxidant-based drugs that can enhance neural cell survival and improve recovery after stroke. However, several groups have demonstrated success in protecting against stroke by increasing expression of antioxidant enzymes in neural cells. These enzymes, which include but are not limited to enzymes in the glutathione peroxidase, catalase, and superoxide dismutase families, degrade ROS that otherwise damage cellular components such as DNA, proteins, and lipids. Several groups have identified cellular therapies including neural stem cells and human umbilical cord blood cells, which exert neuroprotective and oligoprotective effects through the release of pro-survival factors that activate PI3K/Akt signaling to upregulation of antioxidant enzymes. Other studies demonstrate that treatment with soluble factors released by these cells yield similar changes in enzyme expression after stroke. Treatment with the cytokine leukemia inhibitory factor increases the expression of peroxiredoxin IV and metallothionein III in glia and boosts expression of superoxide dismutase 3 in neurons. Through cell-specific upregulation of these enzymes, LIF and other Akt-inducing factors have the potential to protect multiple cell types against damage from ROS during the early and late phases of ischemic damage.
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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.