{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,1]],"date-time":"2026-10-01T09:54:26Z","timestamp":1790848466359,"version":"4.1.0"},"reference-count":75,"publisher":"Ovid Technologies (Wolters Kluwer Health)","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["ATVB"],"abstract":"<jats:sec>\n                    <jats:title>BACKGROUND:<\/jats:title>\n                    <jats:p>Metabolic dysfunction-associated steatotic liver disease (MASLD) is a growing health concern given rising global prevalence, limited diagnostic and therapeutic tools, and strong association with cardiovascular disease. Platelets and oxidized phospholipids have been implicated in MASLD pathogenesis; however, the drivers and activities of platelets in MASLD remain overlooked.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>METHODS:<\/jats:title>\n                    <jats:p>\n                      We conducted a cross-sectional study to determine platelet metabolic and functional states in MASLD and to investigate whether oxidized phospholipids, which accumulate during MASLD, contribute to platelet dysfunction. The study included age-matched individuals with simple steatosis (n=42), steatohepatitis (n=28), metabolic dysfunction-associated cirrhosis (n=16), and controls without steatosis (n=23). Platelet function and metabolism were characterized by flow cytometry and Seahorse analysis. In vivo markers of platelet activation and plasma oxidized low-density lipoprotein were quantified by ELISA. The causal relationship between oxidized phospholipids and the platelet phenotype was investigated by comparing Ldlr\n                      <jats:sup>\u2212\/\u2212<\/jats:sup>\n                      mice fed an Amylin Liver NASH diet to Amylin Liver NASH-fed E06-scFv\/Ldlr\n                      <jats:sup>\u2212\/\u2212<\/jats:sup>\n                      , transgenic mice that express a natural antibody (E06) that neutralizes oxidized phospholipids.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>RESULTS:<\/jats:title>\n                    <jats:p>We report that, since early MASLD in vivo markers of platelet secretion were elevated in plasma and platelets displayed a heightened metabolic activity. In advanced MASLD, associated with MASH and cirrhosis, platelets were refractory to G-protein-coupled receptor stimulation, but more responsive to GPVI stimulation, promoting a secretory and procoagulant phenotype. Platelet dysfunction correlated with increased platelet mitochondrial activity and with blood levels of oxidized low-density lipoprotein, a major source of oxidized lipids. Ex vivo, the oxidized phospholipid oxPAPC recapitulated the increased mitochondrial activity and functional reprogramming observed in MASH platelets. In a mouse model of MASLD, neutralization of oxidized phospholipids partially mitigated diet-induced platelet dysfunction and binding to liver macrophages.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>CONCLUSIONS:<\/jats:title>\n                    <jats:p>In MASLD, we observed heightened platelet metabolic activity and changes in platelet reactivity, providing the basis to target platelet dysfunction for preventing hepatic and extra-hepatic complications of MASLD.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>REGISTRATION:<\/jats:title>\n                    <jats:p>\n                      URL:\n                      <jats:ext-link xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" ext-link-type=\"uri\" xlink:href=\"https:\/\/www.clinicaltrials.gov\">https:\/\/www.clinicaltrials.gov<\/jats:ext-link>\n                      ; Unique identifier: NCT05128253.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1161\/atvbaha.126.325001","type":"journal-article","created":{"date-parts":[[2026,10,1]],"date-time":"2026-10-01T09:00:18Z","timestamp":1790845218000},"update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":0,"title":["Hypermetabolic State Drives Platelet Dysfunction in Human and Mouse Metabolic Dysfunction-Associated Steatotic Liver Disease"],"prefix":"10.1161","clinical-trial-number":[{"clinical-trial-number":"nct05128253","registry":"10.18810\/clinical-trials-gov"}],"author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-5412-5760","authenticated-orcid":true,"given":"Francesca","family":"Maiorca","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-0516-6662","authenticated-orcid":true,"given":"Annamaria","family":"Sabetta","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-0936-8843","authenticated-orcid":true,"given":"Moris","family":"Sangineto","sequence":"additional","affiliation":[{"name":"Liver Unit and Internal Medicine Unit, Department of Medical and Surgical Sciences, University of Foggia, Italy (M.S., M.C., G. 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