ArticleInternational journal of biological sciences2024
Interaction Between the PERK/ATF4 Branch of the Endoplasmic Reticulum Stress and Mitochondrial One-Carbon Metabolism Regulates Neuronal Survival After Intracerebral Hemorrhage.
Article in International journal of biological sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed.
- The role of ATF4 in neurons under mitochondrial stress.NAR genomics and bioinformatics · 2026Article
- Targeting the Mechanosensitive Channel Piezo2 Alleviates Intracerebral Hemorrhage-induced Brain Injury by Modulating ER Stress.Translational stroke research · 2026Article
- Organelle regulation of ferroptosis after intracerebral hemorrhage.Redox biology · 2026Review
- MTHFD2 modulates neural stem cell proliferation and apoptosis after intracerebral hemorrhage by regulating mitochondrial NADPH homeostasis.Journal of translational medicine · 2026Article
- Ironing out mechanisms of ferroptotic death to tailor new stroke therapies.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2026Review
- The dual role of ATF4 in neurons: from stress adaptation to therapeutic intervention.Frontiers in molecular neuroscience · 2026Review
- Mitochondrial dysfunction in intracerebral hemorrhage: molecular mechanisms and pathological consequences.Frontiers in cellular neuroscience · 2026Review
- Novel Phosphatase SSU72 Drives Malignant Progression in Colorectal Cancer via PERKInternational journal of biological sciences · 2026Article
- The dual role of endoplasmic reticulum stress in cerebral ischemia: from adaptive protection to apoptotic induction.Frontiers in molecular neuroscience · 2026Review
- Microglial STING activation promotes neuroinflammation and pathological changes in experimental mice with intracerebral haemorrhage.Acta pharmacologica Sinica · 2025Article
- Farnesol Improves Endoplasmic Reticulum Stress and Hepatic Metabolic Dysfunction Induced by Tunicamycin in Mice.Biology · 2025Article
- Identification of novel gut microbiota-related biomarkers in cerebral hemorrhagic stroke.Frontiers in medicine · 2025Article
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Authors and funding
11 authors.
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Abstract
Recent investigations have revealed that oxidative stress can lead to neuronal damage and disrupt mitochondrial and endoplasmic reticulum functions after intracerebral hemorrhage (ICH). However, there is limited evidence elucidating their role in maintaining neuronal homeostasis. Metabolomics analysis, RNA sequencing, and CUT&Tag-seq were performed to investigate the mechanism underlying the interaction between the PERK/ATF4 branch of the endoplasmic reticulum stress (ERS) and mitochondrial one-carbon (1C) metabolism during neuronal resistance to oxidative stress. The association between mitochondrial 1C metabolism and the PERK/ATF4 branch of the ERS after ICH was investigated using transcription factor motif analysis and co-immunoprecipitation. The findings revealed interactions between the GRP78/PERK/ATF4 and mitochondrial 1C metabolism, which are important in preserving neuronal homeostasis after ICH. ATF4 is an upstream transcription factor that directly regulates the expression of 1C metabolism genes. Additionally, the GRP78/PERK/ATF4 forms a negative regulatory loop with MTHFD2 because of the interaction between GRP78 and MTHFD2. This study presents evidence of disrupted 1C metabolism and the occurrence of ERS in neurons post-ICH. Supplementing exogenous NADPH or interfering with the PERK/ATF4 could reduce symptoms related to neuronal injuries, suggesting new therapeutic prospects for ICH.
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