ArticleAging cell2023
High plasma concentrations of acyl-coenzyme A binding protein (ACBP) predispose to cardiovascular disease: Evidence for a phylogenetically conserved proaging function of ACBP.
Article in Aging cell, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 40 citations in OpenAlex.
- Heart failure in the elderly: epidemiology, mechanisms, and management.European heart journal · 2026Review
- Cell death-induced release of the pro-aging protein acyl CoA binding protein (ACBP) into the circulation.Cell death and differentiation · 2026Article
- Acyl-CoA-binding protein (ACBP): a poor-prognosis biomarker in sepsis and a target for disease mitigation.Signal transduction and targeted therapy · 2026Article
- Neutralization of acyl-CoA-binding protein attenuates glucocorticoid-mediated suppression of cancer immunosurveillance.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Article
- Stress management by benzodiazepines in septic shock and critical illness: mechanistic and clinical evidence supporting alternative sedative strategies.Cell stress · 2026Article
- Benzodiazepines interfere with the efficacy of pembrolizumab-based cancer immunotherapy. Results of a nationwide cohort study including over 50,000 participants with advanced lung cancer.Oncoimmunology · 2025Article
- Potent immune-dependent anticancer effects of the non-cardiotoxic anthracycline aclarubicin.Oncoimmunology · 2025Review
- ACBP/DBI neutralization for the prevention and treatment of malignant and non-malignant liver diseases.Cell death & disease · 2025Review
- Increased plasma concentrations of acyl-coenzyme A binding protein (ACBP) predict future lung cancer development in smokers at risk of cardiovascular disease.Molecular cancer · 2025Article
- Anti-ageing interventions for the treatment of cardiovascular disease.Cardiovascular research · 2025Review
- Roadmap for alleviating the manifestations of ageing in the cardiovascular system.Nature reviews. Cardiology · 2025Review
- Neutralization of acyl CoA binding protein (ACBP) for the experimental treatment of osteoarthritis.Cell death and differentiation · 2025Article
- Hindbrain octadecaneuropeptide gliotransmission as a therapeutic target for energy balance control without nausea or emesis.Science translational medicine · 2025Article
- Neutralization of acyl coenzyme A binding protein for the experimental prevention and treatment of hepatocellular carcinoma.Cell reports. Medicine · 2025Article
- Acyl-CoA-binding protein as a driver of pathological aging.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Review
- ACBP/DBI neutralization for the experimental treatment of fatty liver disease.Cell death and differentiation · 2025Article
- Atlas of expression of acyl CoA binding protein/diazepam binding inhibitor (ACBP/DBI) in human and mouse.Cell death & disease · 2025Article
- ACBP orchestrates the metabolic phenotype in Cushing's syndrome.Nature metabolism · 2024Article
Corrections and comments
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Authors and funding
17 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Autophagy defects accelerate aging, while stimulation of autophagy decelerates aging. Acyl-coenzyme A binding protein (ACBP), which is encoded by a diazepam-binding inhibitor (DBI), acts as an extracellular feedback regulator of autophagy. As shown here, knockout of the gene coding for the yeast orthologue of ACBP/DBI (ACB1) improves chronological aging, and this effect is reversed by knockout of essential autophagy genes (ATG5, ATG7) but less so by knockout of an essential mitophagy gene (ATG32). In humans, ACBP/DBI levels independently correlate with body mass index (BMI) as well as with chronological age. In still-healthy individuals, we find that high ACBP/DBI levels correlate with future cardiovascular events (such as heart surgery, myocardial infarction, and stroke), an association that is independent of BMI and chronological age, suggesting that ACBP/DBI is indeed a biomarker of "biological" aging. Concurringly, ACBP/DBI plasma concentrations correlate with established cardiovascular risk factors (fasting glucose levels, systolic blood pressure, total free cholesterol, triglycerides), but are inversely correlated with atheroprotective high-density lipoprotein (HDL). In mice, neutralization of ACBP/DBI through a monoclonal antibody attenuates anthracycline-induced cardiotoxicity, which is a model of accelerated heart aging. In conclusion, plasma elevation of ACBP/DBI constitutes a novel biomarker of chronological aging and facets of biological aging with a prognostic value in cardiovascular disease.
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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.