ArticleNeurotoxicity research2018
Temporal Pattern and Crosstalk of Necroptosis Markers with Autophagy and Apoptosis Associated Proteins in Ischemic Hippocampus.
Article in Neurotoxicity research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 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.
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Who cites it
24 citing papers in PubMed, 35 citations in OpenAlex.
- Insights on the crosstalk among different cell death mechanisms.Cell death discovery · 2025Review
- Insight into interplay between PANoptosis and autophagy: novel therapeutics in ischemic stroke.Frontiers in molecular neuroscience · 2024Review
- The Role of Induced Pluripotent Stem Cells in the Treatment of Stroke.Current neuropharmacology · 2024Review
- Dexmedetomidine alleviates cerebral ischemia-reperfusion injury via inhibiting autophagy through PI3K/Akt/mTOR pathway.Journal of molecular histology · 2023Article
- Novel insight into cGAS-STING pathway in ischemic stroke: from pre- to post-disease.Frontiers in immunology · 2023Review
- Necroptosis Blockade Potentiates the Neuroprotective Effect of Hypothermia in Neonatal Hypoxic-Ischemic Encephalopathy.Biomedicines · 2022Article
- Article
- Chronic high-fat diet consumption exacerbates pyroptosis- and necroptosis-mediated HMGB1 signaling in the brain after ischemia and reperfusion injury.Journal of physiology and biochemistry · 2022Article
- Necroptosis: A Pathogenic Negotiator in Human Diseases.International journal of molecular sciences · 2022Review
- Do pyroptosis, apoptosis, and necroptosis (PANoptosis) exist in cerebral ischemia? Evidence from cell and rodent studies.Neural regeneration research · 2022Article
- Research progress on astrocyte autophagy in ischemic stroke.Frontiers in neurology · 2022Review
- Pomelo peel oil suppresses TNF-α-induced necroptosis and cerebral ischaemia-reperfusion injury in a rat model of cardiac arrest.Pharmaceutical biology · 2021Article
- How cytosolic compartments play safeguard functions against neuroinflammation and cell death in cerebral ischemia.Metabolic brain disease · 2021Review
- Hypoxic postconditioning-induced neuroprotection increases neuronal autophagy via activation of the SIRT1/FoxO1 signaling pathway in rats with global cerebral ischemia.Experimental and therapeutic medicine · 2021Article
- Insight into Crosstalk between Ferroptosis and Necroptosis: Novel Therapeutics in Ischemic Stroke.Oxidative medicine and cellular longevity · 2021Review
- Mitochondrial Mechanisms of Necroptosis in Liver Diseases.International journal of molecular sciences · 2020Review
- MiR-211 protects cerebral ischemia/reperfusion injury by inhibiting cell apoptosis.Bioengineered · 2020Article
- Adiponectin inhibits cardiac arrest/cardiopulmonary resuscitation‑induced apoptosis in brain by increasing autophagy involved in AdipoR1‑AMPK signaling.Molecular medicine reports · 2020Article
- Small extracellular vesicles secreted by human iPSC-derived MSC enhance angiogenesis through inhibiting STAT3-dependent autophagy in ischemic stroke.Stem cell research & therapy · 2020Article
- Green Tea Polyphenols Modulated Cerebral SOD Expression and Endoplasmic Reticulum Stress in Cardiac Arrest/Cardiopulmonary Resuscitation Rats.BioMed research international · 2020Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Necroptosis, a novel type of programmed cell death, has been recently implicated as a possible mechanism for cerebral ischemia-reperfusion (I/R) injury. We herein studied time-dependent changes of necroptosis markers along with apoptosis- and autophagy-associated proteins in rat hippocampus at 1, 3, 6, 12, 24, and 48 h after global cerebral I/R injury. Furthermore, to determine the cross talk between autophagy and necroptosis, we examined the effects of pretreatment with bafilomycin-A1 (Baf-A1), as a late-stage autophagy inhibitor, on necroptosis. Highest levels of receptor-interacting protein 1 and 3 (RIP1 and RIP3), as key mediators of necroptosis, were observed at 24 h after reperfusion. Alongside, activity of glutamate dehydrogenase (GLUD1), downstream enzyme of RIP3, was increased. Peak time of necroptosis was subsequent to caspase-3-dependent cell death that peaked at 12 h of reperfusion but concurrent with autophagy. Administration of Baf-A1 could attenuate necroptosis, verified by decrease in RIP1 and RIP3 protein levels, as well as GLUD1 activity. However, there was no significant change in caspase-3-dependent cell death. Taken together, our results highlight that global cerebral I/R activates necroptosis that could be triggered by autophagy and interacts reversely with caspase-3-dependent apoptosis.
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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.