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This condition is strongly associated with the risk of cardiovascular disease (CVD), but how MAFLD affects the development and progression of CVD, particularly concerning vascular calcification, remains unclear. Herein, extracellular vesicles (EVs) are identified from steatotic hepatocytes as a trigger that accelerated the progression of both vascular intimal and medial calcification. Steatotic hepatocytes are found to release more EVs, which are able to reach the vascular tissue, be taken up by vascular smooth muscle cells (VSMCs), and promote their osteogenic differentiation. Within these toxic vesicles, a protein cargo is identified called lectin galactoside\u2010binding soluble 3 binding protein (Lgals3bp) that acted as a potent inducer of osteochondrogenic transformation in VSMCs. Both the inhibition of EV release and the liver\u2010specific knockdown of Lgals3bp profoundly attenuated vascular calcification. This work partially explains the reason for the high incidence of vascular calcification in MAFLD and unveils a novel mechanism that may be used to prevent or treat cardiovascular complications in patients with MAFLD.<\/jats:p>","DOI":"10.1002\/advs.202408660","type":"journal-article","created":{"date-parts":[[2024,12,16]],"date-time":"2024-12-16T14:04:38Z","timestamp":1734357878000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":7,"title":["Hepatic Steatosis Aggravates Vascular Calcification via Extracellular Vesicle\u2010Mediated Osteochondrogenic Switch of Vascular Smooth Muscle Cells"],"prefix":"10.1002","volume":"12","author":[{"given":"Zhao\u2010Lin","family":"Zeng","sequence":"first","affiliation":[{"name":"Department of Metabolism and Endocrinology The First Affiliated Hospital, Hengyang Medical School University of South China  Hengyang Hunan 421001 P. R. 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