ArticleFrontiers in molecular neuroscience2020
Targeting Oxidative Stress and Inflammation to Prevent Ischemia-Reperfusion Injury.
Article in Frontiers in molecular neuroscience, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 290 papers, 1 of them a synthesis that pooled it.
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Who cites it
290 citing papers in PubMed, 1 synthesis or guideline pooled it, 483 citations in OpenAlex.
- The Effects of Cannabinoids on Ischemic Stroke-Associated Neuroinflammation: A Systematic Review.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2025Pooled it
- Trial
- Risk factors of cervical anastomotic stricture after esophagectomy detected by early postoperative endoscopy.Surgical endoscopy · 2026Article
- Efficacy and safety of edaravone dexborneol in acute ischemic stroke patients undergoing endovascular thrombectomy: a systematic review and meta-analysis.Naunyn-Schmiedeberg's archives of pharmacology · 2026Review
- Regulation of G Protein Signaling 14 protects against cerebral ischemic reperfusion injury by inhibiting the TAK1-JNK/p38 signaling pathway.Histology and histopathology · 2026Article
- Neuroprotection after transient middle cerebral artery occlusion in male rats using kojic acid nanostructured lipid carriers: A behavioral, biochemical, and histological study on hippocampal CA1 region.Animal models and experimental medicine · 2026Article
- HMGB1 as a danger signal in vascular remodeling.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2026Review
- Activation of cGAS-STING axis by CO@OMVs promote macrophage mitophagy for CIRI treatment.APL bioengineering · 2026Article
- Evaluation of Early and Delayed Meloxicam Treatment Against Regulated Cell Death Pathways and ERK1/2 Phosphorylation in a Rat Model of Renal Ischemia-Reperfusion Injury.Biomedicines · 2026Article
- Protective Effects of Ranolazine in a Rat Model of Ovarian Ischemia/Reperfusion Injury.International journal of molecular sciences · 2026Article
- Imeglimin confers protection against intestinal ischemia/reperfusion injury in rats through AMPK-dependent inhibition of NF-κB/NLRP3 inflammasome signaling and mitigation of oxidative stress and apoptosis.Inflammopharmacology · 2026Article
- Potential of Saliva in Stroke Patients: A Review.International journal of molecular sciences · 2026Review
- Reduced Cerebral Infarct Volume in Young UCP2Cells · 2026Article
- Evaluation of the Nrf2-Keap1 Pathway in Patients with Acute Cerebral Ischemic Disease.Medicina (Kaunas, Lithuania) · 2026Article
- Article
- BTG2 knockdown attenuates oxygen-glucose deprivation/reoxygenation-induced injury and apoptosis in PC12 cells: an effect associated with MAPK pathway inhibition.Molecular biology reports · 2026Article
- Pathological mechanisms and therapeutic potential of MSC-Exos in ischemic stroke management.Stem cell research & therapy · 2026Review
- Gadd45α silencing alleviates cerebral ischemia-reperfusion injury by suppressing FOXO1 signaling.Scientific reports · 2026Article
- Glycitin Alleviates Myocardial Ischemia-reperfusion Injury By Suppressing Oxidative Stress and Apoptosis Through PI3K/Akt/NF-κB Pathway Modulation.Applied biochemistry and biotechnology · 2026Article
- Preventive Effect of Gallic Acid-Loaded Carrageenan Nanoparticles Against Cerebral Ischemia/Reperfusion Injury in Rat: Modulation of Oxidative Pathway.Food science & nutrition · 2026Article
230 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The cerebral ischemia injury can result in neuronal death and/or functional impairment, which leads to further damage and dysfunction after recovery of blood supply. Cerebral ischemia/reperfusion injury (CIRI) often causes irreversible brain damage and neuronal injury and death, which involves many complex pathological processes including oxidative stress, amino acid toxicity, the release of endogenous substances, inflammation and apoptosis. Oxidative stress and inflammation are interactive and play critical roles in ischemia/reperfusion injury in the brain. Oxidative stress is important in the pathological process of ischemic stroke and is critical for the cascade development of ischemic injury. Oxidative stress is caused by reactive oxygen species (ROS) during cerebral ischemia and is more likely to lead to cell death and ultimately brain death after reperfusion. During reperfusion especially, superoxide anion free radicals, hydroxyl free radicals, and nitric oxide (NO) are produced, which can cause lipid peroxidation, inflammation and cell apoptosis. Inflammation alters the balance between pro-inflammatory and anti-inflammatory factors in cerebral ischemic injury. Inflammatory factors can therefore stimulate or exacerbate inflammation and aggravate ischemic injury. Neuroprotective therapies for various stages of the cerebral ischemia cascade response have received widespread attention. At present, neuroprotective drugs mainly include free radical scavengers, anti-inflammatory agents, and anti-apoptotic agents. However, the molecular mechanisms of the interaction between oxidative stress and inflammation, and their interplay with different types of programmed cell death in ischemia/reperfusion injury are unclear. The development of a suitable method for combination therapy has become a hot topic.
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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.