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The evolution of foam cells is not only a significant pathological change in the early stage of atherosclerosis\u00a0but also a key stage\u00a0in the occurrence and development of atherosclerosis. The formation of foam cells is mainly caused by the imbalance among lipids uptake, lipids treatment, and reverse cholesterol transport. Although a large number of studies have summarized the source of foam cells and the mechanism of foam cells formation, we propose a\u00a0new idea\u00a0about foam cells in atherosclerosis. Rather than an isolated microenvironment,\u00a0the macrophage multiple lipid\u00a0uptake pathways, lipid\u00a0internalization, lysosome, mitochondria, endoplasmic reticulum, neutral cholesterol ester hydrolase (NCEH), acyl\u2010coenzyme A\u2013cholesterol acyltransferase (ACAT), and reverse cholesterol transport are mutually influential, and\u00a0form\u00a0a dynamic process under multi\u2010factor regulation. The macrophage takes on different uptake lipid\u00a0statuses depending on multiple uptake pathways and intracellular lipids, lipid metabolites versus pro\u2010inflammatory factors. Except for NCEH and ACAT, the lipid internalization of macrophages also depends on multicellular organelles including the lysosome, mitochondria, and endoplasmic reticulum, which are associated with each other. A dynamic balance between esterification and hydrolysis of cholesterol for macrophages is\u00a0essential for physiology and pathology. Therefore, we propose that the foam cell in the process of atherosclerosis may be dynamic\u00a0under multi\u2010factor regulation, and collate this\u00a0study to provide a holistic and dynamic idea of\u00a0the foam cell.<\/jats:p>","DOI":"10.1002\/jcp.30300","type":"journal-article","created":{"date-parts":[[2021,1,29]],"date-time":"2021-01-29T00:37:33Z","timestamp":1611880653000},"page":"6154-6167","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":47,"title":["Novel insights: Dynamic foam cells derived\u00a0from the macrophage in atherosclerosis"],"prefix":"10.1002","volume":"236","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-1161-8490","authenticated-orcid":false,"given":"Jun","family":"Li","sequence":"first","affiliation":[{"name":"Jiangsu Key Laboratory for Pharmacology and Safety Evaluation of Chinese Materia Medica, School of Pharmacy Nanjing University of Chinese Medicine  Nanjing 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