ArticleCNS neuroscience & therapeutics2017
Roles of autophagy and endoplasmic reticulum stress in intracerebral hemorrhage-induced secondary brain injury in rats.
Article in CNS neuroscience & therapeutics, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed, 69 citations in OpenAlex.
- Organelle regulation of ferroptosis after intracerebral hemorrhage.Redox biology · 2026Review
- Microglia‑mediated neuroinflammation in intracerebral hemorrhage: Pathological mechanisms and implications for therapeutic development (Review).International journal of molecular medicine · 2026Review
- Review
- m6A reader YTHDC2 mediates NCOA4 mRNA stability affecting ferritinophagy to alleviate secondary injury after intracerebral haemorrhage.Epigenetics · 2024Article
- Transcriptomic analysis reveals novel hub genes associated with astrocyte autophagy in intracerebral hemorrhage.Frontiers in aging neuroscience · 2024Article
- A crosstalk between autophagy and apoptosis in intracerebral hemorrhage.Frontiers in cellular neuroscience · 2024Review
- Integrative transcriptomic and network pharmacology analysis reveals the neuroprotective role of BYHWD through enhancing autophagy by inhibiting Ctsb in intracerebral hemorrhage mice.Chinese medicine · 2023Article
- Prognostic potential of serum mesencephalic astrocyte-derived neurotrophic factor in acute intracerebral hemorrhage: a prospective observational study.BMC neurology · 2023Observational
- The Regulated Cell Death and Potential Interventions in Preterm Infants after Intracerebral Hemorrhage.Current neuropharmacology · 2023Review
- [Suppression of HMGB1 inhibits neuronal autophagy and apoptosis to improve neurological deficits in rats following intracerebral hemorrhage].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2022Article
- Role and mechanism of ferroptosis in neurological diseases.Molecular metabolism · 2022Review
- ER Stress is Involved in Mast Cells Degranulation via IRE1α/miR-125/Lyn Pathway in an Experimental Intracerebral Hemorrhage Mouse Model.Neurochemical research · 2022Article
- Chrysophanol Ameliorates Hemin-Induced Oxidative Stress and Endoplasmic Reticulum Stress by Regulating MicroRNA-320-5p/Wnt3a Pathway in HT22 Cells.Oxidative medicine and cellular longevity · 2022Article
- Modes of Brain Cell Death Following Intracerebral Hemorrhage.Frontiers in cellular neuroscience · 2022Review
- Oxidative Stress Following Intracerebral Hemorrhage: From Molecular Mechanisms to Therapeutic Targets.Frontiers in immunology · 2022Review
- Inhibiting Microglia-Derived NLRP3 Alleviates Subependymal Edema and Cognitive Dysfunction in Posthemorrhagic Hydrocephalus after Intracerebral Hemorrhage via AMPK/Beclin-1 Pathway.Oxidative medicine and cellular longevity · 2022Article
- New insights into the interplay between autophagy and oxidative and endoplasmic reticulum stress in neuronal cell death and survival.Frontiers in cell and developmental biology · 2022Review
- Neuroinflammation of microglia polarization in intracerebral hemorrhage and its potential targets for intervention.Frontiers in molecular neuroscience · 2022Review
- Orexin-A exerts neuroprotective effect in experimental intracerebral hemorrhage by suppressing autophagyFrontiers in cellular neuroscience · 2022Article
- Autophagy regulates inflammation in intracerebral hemorrhage: Enemy or friend?Frontiers in cellular neuroscience · 2022Review
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectivesThis study aimed to evaluate the roles of autophagy and endoplasmic reticulum (ER) stress in intracerebral hemorrhage (ICH)-induced secondary brain injury (SBI) in rats.
methodsAutophagy inducer (rapamycin) and inhibitor (3-methyladenine), as well as ER stress activator (tunicamycin, TM) and inhibitor (tauroursodeoxycholic acid, TUDCA), were used. Bafilomycin A1, an inhibitor of autophagosome-lysosome fusion, was used to assess autophagic flux.
resultsAutophagy and ER stress were enhanced in the week after ICH. At 6 hours after ICH, autophagy was excessive, while the autophagic flux was damaged at 72 hours and return to be intact at 7 days after ICH. At 6 hours after ICH, ER stress induction by TM could enhance autophagy and lead to caspase 12-mediated apoptosis and neuronal degeneration, which was further aggravated by autophagy induction. At 7 days after ICH, ER stress inhibition by TUDCA still could suppress ICH-induced SBI. And, the effects of TUDCA were enhanced by autophagy induction.
conclusionsAt 6 hours after ICH, excessive autophagy may participate in ER stress-induced brain injury; at 7 days after ICH, autophagy could enhance the protection of ER stress inhibitor possibly via clearing up the cell rubbish generated due to the early-stage damaged autophagic flux.
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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.