{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,11,10]],"date-time":"2025-11-10T21:22:36Z","timestamp":1762809756593,"version":"3.41.2"},"reference-count":156,"publisher":"American Association for the Advancement of Science (AAAS)","issue":"896","content-domain":{"domain":["www.science.org"],"crossmark-restriction":true},"short-container-title":["Sci. Signal."],"published-print":{"date-parts":[[2025,7,22]]},"abstract":"<jats:p>\n            Cardiomyocytes (CMs) normally use fatty acid oxidation (FAO) as their primary energy source. In response to pathological stress, the substrate preference of CMs switches from FAO to glucose metabolism, leading to the development of heart failure. Obesity increases this pathological risk of cardiovascular disease. We focused on protein tyrosine phosphatase 1B (PTP1B), an inhibitor of insulin signaling, the abundance and activity of which are increased in brain, muscle, and adipose tissues in obese and\/or diabetic animals and in obese human patients. We generated mice with CM-specific deficiency in PTP1B (\n            <jats:italic>\n              PTP1B\n              <jats:sup>fl\/fl<\/jats:sup>\n              ::\uab64MHC\n              <jats:sup>Cre\/+<\/jats:sup>\n            <\/jats:italic>\n            ) to investigate the CM-specific role of PTP1B in response to cardiac dysfunction induced by high-fat diet (HFD) feeding. Although no physiological or functional cardiac differences were observed at baseline,\n            <jats:italic>\n              PTP1B\n              <jats:sup>fl\/fl<\/jats:sup>\n              ::\uab64MHC\n              <jats:sup>Cre\/+<\/jats:sup>\n            <\/jats:italic>\n            mice were protected against development of cardiac hypertrophy, mitochondrial dysfunction, and cardiac steatosis induced by HFD feeding. Metabolomics data revealed that hearts with CM-specific deletion of PTP1B had increased FAO and lipolysis but reduced glucose metabolism. Furthermore, phosphoproteomics analyses and mechanistic studies identified an axis involving the kinases PKM2 and AMPK downstream of PTP1B in the heart, which collectively acted to promote FAO and suppress lipogenesis. Together, these results suggest that CM-specific deletion of PTP1B prevents a substrate switch from FAO to glucose metabolism, protecting the heart against the development of HFD-induced cardiac hypertrophy and dysfunction.\n          <\/jats:p>","DOI":"10.1126\/scisignal.adp6006","type":"journal-article","created":{"date-parts":[[2025,7,22]],"date-time":"2025-07-22T17:58:18Z","timestamp":1753207098000},"update-policy":"https:\/\/doi.org\/10.34133\/aaas_crossmark","source":"Crossref","is-referenced-by-count":1,"title":["Deletion of PTP1B in cardiomyocytes alters cardiac metabolic signaling to protect against cardiomyopathy induced by a high-fat diet"],"prefix":"10.1126","volume":"18","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-8776-0832","authenticated-orcid":true,"given":"Yan","family":"Sun","sequence":"first","affiliation":[{"name":"Department of Biomedical Research and Translational Medicine, Masonic Medical Research Institute, Utica, NY 13501, USA."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Abhishek Kumar","family":"Mishra","sequence":"additional","affiliation":[{"name":"Department of Biomedical Research and Translational Medicine, Masonic Medical Research Institute, Utica, NY 13501, USA."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Vasanth","family":"Chanrasekhar","sequence":"additional","affiliation":[{"name":"Division of Cardiology, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02115, USA."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0009-0009-3131-2887","authenticated-orcid":true,"given":"Michaela","family":"Door","sequence":"additional","affiliation":[{"name":"Department of Cell and Molecular Physiology, Loyola University Chicago Stritch School of Medicine, Maywood, IL 60153, USA."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-2711-0069","authenticated-orcid":true,"given":"Chase W.","family":"Kessinger","sequence":"additional","affiliation":[{"name":"Department of Biomedical Research and Translational Medicine, Masonic Medical Research Institute, Utica, NY 13501, USA."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Bing","family":"Xu","sequence":"additional","affiliation":[{"name":"Department of Biomedical Research and Translational Medicine, Masonic Medical Research Institute, Utica, NY 13501, USA."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Peiyang","family":"Tang","sequence":"additional","affiliation":[{"name":"Department of Biomedical Research and Translational Medicine, Masonic Medical Research Institute, Utica, NY 13501, USA."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-4381-4712","authenticated-orcid":true,"given":"Yunan","family":"Gao","sequence":"additional","affiliation":[{"name":"Department of Cardiology, Fourth Affiliated Hospital of Harbin Medical University, 37 Yiyuan Street, Harbin, Heilongjiang 150001, China."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-5107-5366","authenticated-orcid":true,"given":"Sarah","family":"Kamli-Salino","sequence":"additional","affiliation":[{"name":"University of Aberdeen, School of Medicine, Medical Sciences and Nutrition, Institute of Medical Sciences, Aberdeen AB24 3FX, UK."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0009-0002-3131-2616","authenticated-orcid":true,"given":"Katherine","family":"Nelson","sequence":"additional","affiliation":[{"name":"Department of Biomedical Research and Translational Medicine, Masonic Medical Research Institute, Utica, NY 13501, USA."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-6193-3152","authenticated-orcid":true,"given":"Mirela","family":"Delibegovic","sequence":"additional","affiliation":[{"name":"University of Aberdeen, School of Medicine, Medical Sciences and Nutrition, Institute of Medical Sciences, Aberdeen AB24 3FX, UK."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-5290-0738","authenticated-orcid":true,"given":"E. 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