ArticleNeurochemical research2012
Intracellular signaling MAPK pathway after cerebral ischemia-reperfusion injury.
Article in Neurochemical research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
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Who cites it
48 citing papers in PubMed, 83 citations in OpenAlex.
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- Targeting PI3K/Akt in Cerebral Ischemia Reperfusion Injury Alleviation: From Signaling Networks to Targeted Therapy.Molecular neurobiology · 2024Review
- Differential gene expression in the contralateral hemisphere of the rat brain after focal ischemia.Scientific reports · 2023Article
- Role of traditional Chinese medicine monomers in cerebral ischemia/reperfusion injury:a review of the mechanism.Frontiers in pharmacology · 2023Review
- Comparative Use of Contralateral and Sham-Operated Controls Reveals Traces of a Bilateral Genetic Response in the Rat Brain after Focal Stroke.International journal of molecular sciences · 2022Article
- Maslinic Acid Attenuates Ischemia/Reperfusion-Induced Acute Kidney Injury by Suppressing Inflammation and Apoptosis Through Inhibiting NF-κB and MAPK Signaling Pathway.Frontiers in pharmacology · 2022Article
- Cellular Signalling and Photobiomodulation in Chronic Wound Repair.International journal of molecular sciences · 2021Review
- Advancement in research on the role of the transient receptor potential vanilloid channel in cerebral ischemic injury (Review).Experimental and therapeutic medicine · 2021Review
- δ-Opioid receptor activation ameliorates lipopolysaccharide-induced inflammation and apoptosis by inhibiting the MAPK/caspase-3 pathway in BV2 microglial cells.Experimental brain research · 2021Article
- Influence of miR-1 on Nerve Cell Apoptosis in Rats with Cerebral Stroke via Regulating ERK Signaling Pathway.BioMed research international · 2021Article
- The Cerebroprotein Hydrolysate-I Plays a Neuroprotective Effect on Cerebral Ischemic Stroke by Inhibiting MEK/ERK1/2 Signaling Pathway in Rats.Neuropsychiatric disease and treatment · 2021Article
- Protective Effect of Triphala against Oxidative Stress-Induced Neurotoxicity.BioMed research international · 2021Article
- Article
- Inhibition of mast cell tryptase attenuates neuroinflammation via PAR-2/p38/NFκB pathway following asphyxial cardiac arrest in rats.Journal of neuroinflammation · 2020Article
- Scorpion Venom Heat-Resistant Peptide is Neuroprotective against Cerebral Ischemia-Reperfusion Injury in Association with the NMDA-MAPK Pathway.Neuroscience bulletin · 2020Article
- Longshengzhi Capsules Improve Ischemic Stroke Outcomes and Reperfusion Injury via the Promotion of Anti-Inflammatory and Neuroprotective Effects in MCAO/R Rats.Evidence-based complementary and alternative medicine : eCAM · 2020Article
- HMGB1-triggered inflammation inhibition of notoginseng leaf triterpenes against cerebral ischemia and reperfusion injury via MAPK and NF-κB signaling pathways.Biomolecules · 2019Article
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The MAPK/ERK/p38 are signal transduction pathways that couple intracellular responses to the external stimuli. Contrary to ERK protein which is part of the survival route, presence of p38 could have an impact on cell injury. Tolerance induced by ischemic preconditioning (IPC) is a phenomenon of tissue adaptation, which results in increased tolerance to lethal ischemia-reperfusion injury (IRI). Paper describes changes in MAPK protein pathways after brain IPC. Ischemia was induced by 4-vessels occlusion and rats were preconditioned by sub-lethal ischemia. Western blot and immunohistochemistry identified ERK/p38 proteins in injured areas. The highest level of the pERK was detected at 24 h in IPC groups. A contrary pattern of MAPK/p38 activation was observed in this group, where the lowest level of p38 was displayed at 24 h after ischemia. This suggests that the MAPK signal transduction might have a potential role in tissues response subjected to IRI and in the phenomenon of tolerance.
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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.