ArticleCell death & disease2017
RTN1-C mediates cerebral ischemia/reperfusion injury via ER stress and mitochondria-associated apoptosis pathways.
Article in Cell death & disease, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 126 papers, 1 of them a synthesis that pooled it.
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Who cites it
126 citing papers in PubMed, 1 synthesis or guideline pooled it, 267 citations in OpenAlex.
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- Inter-Organelle Membrane Contact Sites as Physiological Regulatory Hubs in the Brain: From Neurons to Glial Cells.Biomolecules · 2026Review
- N6-Methyladenosine Demethylase FTO Mitigates Cerebral Ischemia-Reperfusion Injury by Suppressing AQP4 Expression.CNS neuroscience & therapeutics · 2026Article
- Gut-brain axis modulation by fecal microbiota transplantation improves dual-organ injury after cerebral ischemia-reperfusion via Caspase-8 dependent inhibition of necroptosis.Metabolic brain disease · 2026Article
- Hippocampal Mitochondrial Dysfunction and Synaptic Disruption Link Organophosphate Exposure to Pre-Diabetes: An LC-MS/MS-Based Proteomics Approach.Biomolecules · 2026Article
- Pathological mechanisms and therapeutic potential of MSC-Exos in ischemic stroke management.Stem cell research & therapy · 2026Review
- Endovascular stem cell therapy reconfigures post-stroke ER dynamics via GRP78/Atlastin/CHOP axis.Molecular brain · 2026Article
- Fuzheng Jiedu Tongluo Granule Alleviates Cerebral Ischemia/reperfusion Injury-induced Inflammation By Inhibiting Drp1-mediated TXNIP/NLRP3 Pathway.Molecular neurobiology · 2026Article
- Advances in the mechanisms of electroacupuncture in the treatment of cerebral ischemia-reperfusion injury.Frontiers in neuroscience · 2026Review
- Extracellular Vesicles: a Promising Therapy for Treatment of Central Nervous System Ischemia Reperfusion Injury.Molecular neurobiology · 2025Review
- Emerging Roles of Meningeal Lymphatic Vessels in Ischemic Stroke.Molecular neurobiology · 2025Review
- A Small-Molecule Activator of Sarco/Endoplasmic Reticulum CaACS pharmacology & translational science · 2025Article
- Novel furo[2,3-RSC medicinal chemistry · 2025Article
- Sanggenol L inhibits the HMGB1/TLR4/NF-κB signaling pathway to prevent cerebral ischemia-reperfusion damage.Journal of molecular histology · 2025Article
- Neocarzilin A induces apoptosis and mitochondrial disturbance by targeting reticulon 4-mediated endoplasmic reticulum stress.Cell death discovery · 2025Article
- The role of protein lactylation in brain health and disease: current advances and future directions.Cell death discovery · 2025Review
- Lercanidipine Enhances Cisplatin Activity: Dual Anticancer and Anti-Inflammatory Effects via Caspase Activation and MAPK Inhibition.Pharmaceuticals (Basel, Switzerland) · 2025Article
- TIGAR Suppresses ER Stress-Induced Neuronal Injury through Targeting ATF4 Signaling in Cerebral Ischemia/Reperfusion.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Article
66 more citing papers are in PubMed but not listed here.
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The reticulon family has been found to induce apoptosis, inhibit axon regeneration and regulate protein trafficking. However, little is known about the mechanisms of how reticulon proteins are involved in neuronal death-promoting processes during ischemia. Here, we report that the expression of Reticulon Protein 1-C (RTN1-C) was associated with the progression of cerebral ischemia/reperfusion (I/R) injury. Using a combination of rat middle cerebral artery occlusion (MCAO) stroke and oxygen-glucose deprivation followed by reoxygenation (OGD/R) models, we determined that the expression of RTN1-C was significantly increased during cerebral ischemic/reperfusion. RTN1-C overexpression induced apoptosis and increased the cell vulnerability to ischemic injury, whereas RTN1-C knockdown reversed ischemia-induced apoptosis and attenuated the vulnerability of OGD/R-treated neural cells. Mechanistically, we demonstrated that RTN1-C mediated OGD/R-induced apoptosis through ER stress and mitochondria-associated pathways. RTN1-C interacted with Bcl-xL and increased its localization in the ER, thus reducing the anti-apoptotic activity of Bcl-xL. Most importantly, knockdown of Rtn1-c expression in vivo attenuated apoptosis in MCAO rats and reduced the extent of I/R-induced brain injury, as assessed by infarct volume and neurological score. Collectively, these data support for the first time that RTN1-C may represent a novel candidate for therapies against cerebral ischemia/reperfusion injury.
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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.