{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Montegut L"],"funding":["Equipex","BioTechMed-Graz","Bundesministerium für Bildung, Wissenschaft und Forschung","Association pour la Recherche sur le Cancer","BioHealth, NAWI Graz","Agence Nationale de la Recherche","Institut Universitaire de France","European Commission","Fondation Carrefour","European Union Horizon 2020 Projects Oncobiome and Crimson","Austrian Society of Cardiology","Mark Foundation For Cancer Research","Elior","European Joint Programme on Rare Diseases","Fondation pour la Recherche Médicale","Medizinische Universität Graz","Österreichische Kardiologische Gesellschaft","Ligue Contre le Cancer","Association \"Ruban Rose\"","China Scholarship Council","Austrian Science Fund FWF","SIRIC","Institut National Du Cancer","RHU Torino Lumière","LABEX Immuno-Oncology","Institut National de la Santé et de la Recherche Médicale","Cancéropôle Ile-de-France","Seerave Foundation","Fondation Leducq","IdEx Université de Paris","Odyssea Gustave Roussy"],"pagination":["e13751"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC9835587"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["22(1)"],"pubmed_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."],"journal":["Aging cell"],"pubmed_title":["High plasma concentrations of acyl-coenzyme A binding protein (ACBP) predispose to cardiovascular disease: Evidence for a phylogenetically conserved proaging function of ACBP."],"pmcid":["PMC9835587"],"funding_grant_id":["AMMICa US23/CNRS UMS3655","P29203","ANR-18-IDEX-0001","H2020-MSCA-IF","P27893","DK-MCD W1226","SFB LIPOTOX F3007 & F3012","SFB LIPOTOX F3007 & F3012","P31727","P29262","H2020‐MSCA‐IF","BMWFW‐80.109/0001‐WF/V/3b/2015","équipe labellisée","101025118","DK‐MCD W1226","ASPIRE Award","BMWFW-80.109/0001-WF/V/3b/2015"],"pubmed_authors":["Lachkar S","Lambertucci F","Montegut L","Ruckenstuhl C","Chen H","Blanchet B","Fumeron F","Kroemer G","Maiuri MC","Abdellatif M","Anagnostopoulos G","Dichtinger S","Goldwasser F","Madeo F","Martins I","Joseph A","Motino O"],"additional_accession":[]},"is_claimable":false,"name":"High plasma concentrations of acyl-coenzyme A binding protein (ACBP) predispose to cardiovascular disease: Evidence for a phylogenetically conserved proaging function of ACBP.","description":"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.","dates":{"release":"2023-01-01T00:00:00Z","publication":"2023 Jan","modification":"2025-04-19T12:37:01.311Z","creation":"2025-04-19T12:37:01.311Z"},"accession":"S-EPMC9835587","cross_references":{"pubmed":["36510662"],"doi":["10.1111/acel.13751"]}}