ArticleScientific reports2018
Exercise Mitigates Alcohol Induced Endoplasmic Reticulum Stress Mediated Cognitive Impairment through ATF6-Herp Signaling.
Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 47 citations in OpenAlex.
- The influence of exercise duration on inhibiting endoplasmic reticulum stress in ischemic stroke rats.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2026Article
- Spatial transcriptomics analysis uncovers ER stress in MANF-deficient Purkinje cells underlying alcohol-induced cerebellar neurodegeneration in mice.Acta neuropathologica communications · 2025Article
- Relationship between sedentary time and cognitive decline in hypertensive patients-mediating role of the weight-adjusted waist circumference index.Scientific reports · 2025Article
- Role of Endoplasmic Reticulum Stress-Associated Genes in Septic Neonatal Foals.Antioxidants (Basel, Switzerland) · 2025Article
- Environmental adversity, endoplasmic reticulum stress, and neurogenesis.Neurotoxicology · 2025Review
- Insulin-Like Growth Factor 2 Reverses Synaptic and Cognitive Deficits in Fetal Growth Restriction Mice.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- Article
- Potential molecular mechanism of exercise reversing insulin resistance and improving neurodegenerative diseases.Frontiers in physiology · 2024Review
- Sex-specific effects of alcohol on neurobehavioral performance and endoplasmic reticulum stress: an analysis using neuron-specific MANF deficient mice.Frontiers in pharmacology · 2024Article
- Upregulation of mesencephalic astrocyte-derived neurotrophic factor (MANF) expression offers protection against alcohol neurotoxicity.Journal of neurochemistry · 2023Article
- Pathogenic mechanisms and regulatory factors involved in alcoholic liver disease.Journal of translational medicine · 2023Review
- Article
- Potential Role of MANF, an ER Stress Responsive Neurotrophic Factor, in Protecting Against Alcohol Neurotoxicity.Molecular neurobiology · 2022Review
- Article
- Hydrogen Sulfide (HCurrent neuropharmacology · 2022Review
- The Effect of Chronic Alcohol on Cognitive Decline: Do Variations in Methodology Impact Study Outcome? An Overview of Research From the Past 5 Years.Frontiers in neuroscience · 2022Review
- Mechanism of Blood-Heart-Barrier Leakage: Implications for COVID-19 Induced Cardiovascular Injury.International journal of molecular sciences · 2021Article
- Sustained Inhibition of NF-κB Activity Mitigates Retinal Vasculopathy in Diabetes.The American journal of pathology · 2021Article
- Ethanol Gestational Exposure Impairs Vascular Development and Endothelial Potential to Control BBB-Associated Astrocyte Function in the Developing Cerebral Cortex.Molecular neurobiology · 2021Article
- High Fat Diet Dysbiotic Mechanism of Decreased Gingival Blood Flow.Frontiers in physiology · 2021Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Chronic ethanol/alcohol (AL) dosing causes an elevation in homocysteine (Hcy) levels, which leads to the condition known as Hyperhomocysteinemia (HHcy). HHcy enhances oxidative stress and blood-brain-barrier (BBB) disruption through modulation of endoplasmic reticulum (ER) stress; in part by epigenetic alternation, leading to cognitive impairment. Clinicians have recommended exercise as a therapy; however, its protective effect on cognitive functions has not been fully explored. The present study was designed to observe the protective effects of exercise (EX) against alcohol-induced epigenetic and molecular alterations leading to cerebrovascular dysfunction. Wild-type mice were subjected to AL administration (1.5 g/kg-bw) and subsequent treadmill EX for 12 weeks (5 day/week@7-11 m/min). AL affected mouse brain through increases in oxidative and ER stress markers, SAHH and DNMTs alternation, while decreases in CBS, CSE, MTHFR, tight-junction proteins and cellular H
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Registered trials
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.