{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,26]],"date-time":"2026-10-26T11:28:44Z","timestamp":1793014124227,"version":"4.5.0"},"reference-count":83,"publisher":"National Academy of Sciences","issue":"28","license":[{"start":{"date-parts":[[2025,7,7]],"date-time":"2025-07-07T00:00:00Z","timestamp":1751846400000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by-nc-nd\/4.0\/"}],"content-domain":{"domain":["www.pnas.org"],"crossmark-restriction":true},"short-container-title":["Proc. Natl. Acad. Sci. U.S.A."],"published-print":{"date-parts":[[2025,7,15]]},"abstract":"<jats:p>\n                    The tissue hormone acyl coenzyme A\u2013binding protein (ACBP, encoded by the gene\n                    <jats:italic toggle=\"yes\">diazepam-binding inhibitor<\/jats:italic>\n                    , DBI) has been implicated in various facets of pathological aging. Here, we show that ACBP plasma concentrations are elevated in (close-to-)centenarians (mean \u00b1 SD age 99.5 \u00b1 4.5 y) commensurate with their health deterioration, correlating with a reduced glomerular filtration rate and a surge in senescence-associated cytokines. ACBP neutralization by means of a monoclonal antibody (mAb) improved health span in a strain of progeroid mice. In a mouse model of chronic kidney injury induced by cisplatin, anti-ACBP mAb administration counteracted both histopathological and functional signs of organ failure. ACBP inhibition also prevented the senescence of tubular epithelial cells and glomerular podocytes induced by cisplatin or doxorubicin, respectively, as measurable by the immunohistochemical detection of cyclin-dependent kinase inhibitor 1A (CDKN1A, best known as p21). Senescence was also prevented by anti-ACBP mAb treatment in additional mouse models of accelerated aging. This applied to liver damage induced by a combination of high-fat diet and carbon tetrachloride, where hepatic cells become senescent. Moreover, administration of anti-ACBP mAb prevented natural and doxorubicin-accelerated cardiomyocyte senescence. We performed single-nucleus RNA sequencing to study the transcriptome of hearts that had been exposed to doxorubicin and\/or anti-ACBP in vivo. In cardiomyocytes, doxorubicin caused an anti-ACBP-reversible dysregulation of mRNAs coding for cardioprotective proteins involved in autophagy, fatty acid oxidation, mitochondrial homeostasis, and oxidative phosphorylation. Altogether, these findings plead in favor of a broad age-promoting effect of ACBP across different organ systems.\n                  <\/jats:p>","DOI":"10.1073\/pnas.2501584122","type":"journal-article","created":{"date-parts":[[2025,7,7]],"date-time":"2025-07-07T15:01:13Z","timestamp":1751900473000},"update-policy":"https:\/\/doi.org\/10.1073\/pnas.cm10313","source":"Crossref","is-referenced-by-count":18,"title":["Acyl-CoA-binding protein as a driver of pathological aging"],"prefix":"10.1073","volume":"122","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-4778-4757","authenticated-orcid":false,"given":"L\u00e9a","family":"Mont\u00e9gut","sequence":"first","affiliation":[{"name":"Team Metabolism, Cancer & Immunity, Centre de Recherche des Cordeliers, Equipe Labellis\u00e9e par la Ligue Contre le Cancer, Universit\u00e9 Paris Cit\u00e9, Sorbonne Universit\u00e9, Inserm U1138, Institut Universitaire de France","place":["Paris, France"]},{"name":"Metabolomics and Cell Biology Platforms, Gustave Roussy Institute","place":["Villejuif, France"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Flavia","family":"Lambertucci","sequence":"additional","affiliation":[{"name":"Team Metabolism, Cancer & Immunity, Centre de Recherche des Cordeliers, Equipe Labellis\u00e9e par la Ligue Contre le Cancer, Universit\u00e9 Paris Cit\u00e9, Sorbonne Universit\u00e9, Inserm U1138, Institut Universitaire de France","place":["Paris, France"]},{"name":"Metabolomics and Cell Biology Platforms, Gustave Roussy Institute","place":["Villejuif, France"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0000-5320-489X","authenticated-orcid":false,"given":"Lucas","family":"Moledo-Nodar","sequence":"additional","affiliation":[{"name":"Departamento de Bioqu\u00edmica y Biolog\u00eda Molecular, Instituto Universitario de Oncolog\u00eda, Universidad de Oviedo","place":["Oviedo, 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