ArticleGeroScience2025
Chronic alcohol consumption accelerates cardiovascular aging and decreases cardiovascular reserve capacity.
Article in GeroScience, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
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The trial behind it
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Who cites it
10 citing papers in PubMed.
- PCSK9 inhibition attenuates alcohol-induced cardiovascular dysfunction and links hepatic lipid accumulation to impaired myocardial contractile reserve.GeroScience · 2026Article
- Targeted clearance of senescent cells alleviates alcohol-associated liver disease by restoring cellular function and immune balance.GeroScience · 2026Article
- Alcohol Intake and Incidence of Heart Failure and Its Subtypes: VA Million Veteran Program.Nutrients · 2026Article
- Global burden and projections of cardiometabolic diseases attributable to high alcohol use: a comparative risk assessment based on the GBD 2021 study.Frontiers in nutrition · 2026Article
- Selective Depletion of Gut Gram-Negative Bacteria Attenuates Alcohol Binge-Induced Cardiovascular Dysfunction by Lowering Cardiac Anandamide Levels.The American journal of pathology · 2026Article
- The Link between Alcohol Consumption and Kidney Injury.The American journal of pathology · 2026Review
- Alcohol Consumption and Acute Coronary Syndrome: Epidemiology, Pathophysiology, and Clinical Perspectives.Journal of clinical medicine · 2025Review
- Influence of Exercise on Oxygen Consumption, Pulmonary Ventilation, and Blood Gas Analyses in Individuals with Chronic Diseases.Life (Basel, Switzerland) · 2025Review
- Article
- Global burden and projections of stroke and its subtypes attributable to high alcohol use during 1990-2021: insights from the global burden of disease study 2021.Frontiers in neurology · 2025Article
Corrections and comments
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Authors and funding
7 authors.
Funding
Abstract
The pathology of cardiovascular aging is complex, involving mitochondrial dysfunction, oxidative and nitrative stress, oxidative DNA injury, impaired lipid metabolism, cell death, senescence, and chronic inflammation. These processes lead to remodeling and structural changes in the cardiovascular system, resulting in a progressive decline in cardiovascular reserve capacity and health, and an increased risk of diseases and mortality. Excessive alcohol consumption exacerbates these risks by promoting hypertension, stroke, arrhythmias, coronary artery disease, cardiomyopathy, and sudden cardiac death, yet the effects of chronic alcohol consumption on cardiovascular aging remain unclear. Herein, we explored the impact of a 6-month 5% Lieber-DeCarli alcohol diet in young (3 months old) and aging (24-26 months old) Fisher F344BNF1 rats. We assessed detailed hemodynamics, mitochondrial function, oxidative/nitrative stress, lipid metabolism, inflammation, cell death, senescence, and myocardial fibrosis using the pressure-volume system, isolated vascular rings, and various histological, biochemical, and molecular biology methods. Alcohol consumption in both young and aging rats impaired mitochondrial function, disrupted cholesterol and triglyceride metabolism, and increased oxidative/nitrative stress, inflammation, cell death, and senescence, leading to a decline in systolic contractile function. In aging rats, alcohol further exacerbated diastolic dysfunction and myocardial fibrosis. Alcohol also increased oxidative/nitrative stress, apoptosis, and senescence in the vasculature, contributing to endothelial dysfunction and increased total peripheral resistance. Additionally, alcohol exacerbated the aging-related ventriculo-arterial uncoupling and diminished cardiac efficiency, further reducing cardiovascular reserve capacity. In conclusion, chronic alcohol consumption promotes cardiovascular aging and further diminishes the already impaired cardiac and vascular reserve capacity associated with aging.
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Registered trials
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