ArticleMolecular and cellular biochemistry2014
The AKT/mTOR pathway mediates neuronal protective effects of erythropoietin in sepsis.
Article in Molecular and cellular biochemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers, 1 of them a synthesis that pooled it.
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Who cites it
38 citing papers in PubMed, 1 synthesis or guideline pooled it, 56 citations in OpenAlex.
- Long-Term Cognitive Outcomes After Sepsis: a Translational Systematic Review.Molecular neurobiology · 2019Pooled it
- Cognitive Impairment in Multiple Sclerosis.Bioengineering (Basel, Switzerland) · 2023Review
- Moderate exercise-induced dynamics on key sepsis-associated signaling pathways in the liver.Critical care (London, England) · 2023Article
- Exploring Neuroprotective Agents for Sepsis-Associated Encephalopathy: A Comprehensive Review.International journal of molecular sciences · 2023Review
- Cellular Metabolism: A Fundamental Component of Degeneration in the Nervous System.Biomolecules · 2023Review
- The impact of aging and oxidative stress in metabolic and nervous system disorders: programmed cell death and molecular signal transduction crosstalk.Frontiers in immunology · 2023Review
- The Metabolic Basis for Nervous System Dysfunction in Alzheimer's Disease, Parkinson's Disease, and Huntington's Disease.Current neurovascular research · 2023Article
- Unravelling the potential neuroprotective facets of erythropoietin for the treatment of Alzheimer's disease.Metabolic brain disease · 2022Review
- Current Understanding of Long-Term Cognitive Impairment After Sepsis.Frontiers in immunology · 2022Review
- Basic research and clinical progress of sepsis-associated encephalopathy.Journal of intensive medicine · 2021Review
- Neurodegeneration, memory loss, and dementia: the impact of biological clocks and circadian rhythm.Frontiers in bioscience (Landmark edition) · 2021Review
- Cognitive Impairment and Dementia: Gaining Insight through Circadian Clock Gene Pathways.Biomolecules · 2021Review
- Sepsis and Cerebral Dysfunction: BBB Damage, Neuroinflammation, Oxidative Stress, Apoptosis and Autophagy as Key Mediators and the Potential Therapeutic Approaches.Neurotoxicity research · 2021Review
- Systemic Response to Infection Induces Long-Term Cognitive Decline: Neuroinflammation and Oxidative Stress as Therapeutical Targets.Frontiers in neuroscience · 2021Review
- New Insights for nicotinamide: Metabolic disease, autophagy, and mTOR.Frontiers in bioscience (Landmark edition) · 2020Review
- lncRNA MALAT1 Accelerates Skeletal Muscle Cell Apoptosis and Inflammatory Response in Sepsis by Decreasing BRCA1 Expression by Recruiting EZH2.Molecular therapy. Nucleic acids · 2020Article
- Dysregulation of metabolic flexibility: The impact of mTOR on autophagy in neurodegenerative disease.International review of neurobiology · 2020Review
- Nicotinamide: Oversight of Metabolic Dysfunction Through SIRT1, mTOR, and Clock Genes.Current neurovascular research · 2020Review
- Synergistic cytoprotection by co-treatment with dexamethasone and rapamycin against proinflammatory cytokine-induced alveolar epithelial cell injury.Journal of intensive care · 2019Article
- Metformin ameliorates sepsis-induced brain injury by inhibiting apoptosis, oxidative stress and neuroinflammation via the PI3K/Akt signaling pathway.Oncotarget · 2017Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Sepsis is one of the most common causes of mortality in intensive care units. Although sepsis-associated encephalopathy (SAE) is reported to be a leading manifestation of sepsis, its pathogenesis remains to be elucidated. In this study, we investigated whether exogenous recombinant human erythropoietin (rhEPO) could protect brain from neuronal apoptosis in the model of SAE. We showed that application of rhEPO enhanced Bcl-2, decreased Bad in lipopolysaccharide treated neuronal cultures, and improved neuronal apoptosis in hippocampus of cecal ligation and peroration rats. We also found that rhEPO increased the expression of phosphorylated AKT, and the antiapoptotic role of rhEPO could be abolished by phosphoinositide 3-kinase (PI3K)/AKT inhibitor LY294002 or SH-5. In addition, systemic sepsis inhibited the hippocampal-phosphorylated mammalian target of rapamycin (mTOR) and p70S6K (downstream substrates of PKB/AKT signaling), which were restored by administration of exogenous rhEPO. Moreover, treatment with mTOR-signaling inhibitor rapamycin or transfection of mTOR siRNA reversed the neuronal protective effects of rhEPO. Finally, exogenous rhEPO rescued the emotional and spatial cognitive defects without any influence on locomotive activity. These results illustrated that exogenous rhEPO improves brain dysfunction by reducing neuronal apoptosis, and AKT/mTOR signaling is likely to be involved in this process. Application of rhEPO may serve as a potential therapy for the treatment of SAE.
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