ArticleAlcoholism, clinical and experimental research2014
Acute alcohol modulates cardiac function as PI3K/Akt regulates oxidative stress.
Article in Alcoholism, clinical and experimental research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 39 citations in OpenAlex.
- Timeless and Stainless Alcohol: Concentric Waves from Its Oxidative Metabolism and Related Oxidative Stress.Antioxidants (Basel, Switzerland) · 2026Review
- Astaxanthin Prevented Acute Alcoholic Cardiomyopathy by Maintenance of Mitophagy-Mediated Mitochondrial Homeostasis.Journal of cellular and molecular medicine · 2025Article
- Sex Difference of Alcoholic Hypertension: Mechanism and Targeted Therapy.Current hypertension reports · 2025Review
- Solid herbal extract ofJournal of traditional and complementary medicine · 2023Article
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- Alcohol Use Disorders and Their Harmful Effects on the Contractility of Skeletal, Cardiac and Smooth Muscles.Advances in drug and alcohol research · 2021Article
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- Ethanol-induced CYP2E1 Expression is Reduced by Lauric Acid via PI3K Pathway in HepG2 Cells.Tropical life sciences research · 2020Article
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- Inflammatory cardiac fibroblast phenotype underlies chronic alcohol-induced cardiac atrophy and dysfunction.Life sciences · 2020Article
- Cardiac Toxicity From Ethanol Exposure in Human-Induced Pluripotent Stem Cell-Derived Cardiomyocytes.Toxicological sciences : an official journal of the Society of Toxicology · 2019Article
- Role of Alcohol Oxidative Metabolism in Its Cardiovascular and Autonomic Effects.Advances in experimental medicine and biology · 2019Review
- Acute alcohol prevents the refeeding-induced decrease in autophagy but does not alter the increased protein synthetic response in heart.Alcohol (Fayetteville, N.Y.) · 2018Article
- Alcoholism: A Multi-Systemic Cellular Insult to Organs.International journal of environmental research and public health · 2018Review
- Alcohol-Mediated Organ Damages: Heart and Brain.Frontiers in pharmacology · 2018Review
- Etiology of alcoholic cardiomyopathy: Mitochondria, oxidative stress and apoptosis.The international journal of biochemistry & cell biology · 2017Review
- Alcoholic Cardiomyopathy: Disrupted Protein Balance and Impaired Cardiomyocyte Contractility.Alcoholism, clinical and experimental research · 2017Review
- Alcohol Induces Cellular Senescence and Impairs Osteogenic Potential in Bone Marrow-Derived Mesenchymal Stem Cells.Alcohol and alcoholism (Oxford, Oxfordshire) · 2017Article
- Low Molecular Weight Heparin Nebulization Attenuates Acute Lung Injury.BioMed research international · 2017Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
backgroundClinical manifestations of alcohol abuse on the cardiac muscle include defective contractility with the development of heart failure. Interestingly, low alcohol consumption has been associated with reduced risk of cardiovascular disease. Although several hypotheses have been postulated for alcoholic cardiomyopathy and for the low-dose beneficial cardiovascular effects, the precise mechanisms and mediators remain largely undefined. We hypothesize that modulation of oxidative stress by PI3K/Akt plays a key role in the cardiac functional outcome to acute alcohol exposure.
methodsThus, acutely exposed rat cardiac tissue and cardiocytes to low (LA: 5 mM), moderate (MA: 25 mM), and high (HA: 100 mM) alcohol were assessed for markers of oxidative stress in the presence and absence of PI3K/Akt activators (IGF-1 0.1 μM or constitutively active PI3K: Ad.BD110 transfection) or inhibitor (LY294002 1 μM or Akt-negative construct Ad.Akt(K179M) transfection).
resultsAcute LA reduced Akt, superoxide dismutase (SOD-3) and NFκB, ERK1, and p38 MAPK gene expression. Acute HA only increased that of SOD-3 and NFκB. These effects were generally inhibited by Ad.Akt(K179M) and enhanced with Ad.BD110 transfection. In parallel, LA reduced but HA enhanced Akt activity, which was reversed by IGF-1 and inhibited by Ad.Akt(K179M), respectively. Also, LA reduced caspase 3/7 activity and oxidative stress, while HA increased both. The former was blocked, while the latter effect was enhanced by Ad.Akt(K179M). The reverse was true with PI3K/Akt activation. This translated into reduced viability with HA, with no effect with LA. On the functional level, acute LA improved cardiac output and ejection fraction, mainly through increased stroke volume. This was accompanied with enhanced end-systolic pressure-volume relationship and preload recruitable stroke work. Opposite effect was recorded for HA. LA and HA in vivo functional effects were alleviated by LY and enhanced by IGF-1 treatment.
conclusionsAcute LA and HA seem to oppositely affect cardiac function through modulation of oxidative stress where PI3K/Akt plays a pivotal role.
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