{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\n In this study, oxidized low-density lipoprotein (ox-LDL) treatment of human umbilical vein endothelial cells (HUVECs) led to the secretion of exosomes enriched with the long non-coding RNA LINC01005 (1). These exosomes were found to promote a phenotype switch in vascular smooth muscle cells (VSMCs), enhancing their proliferation and migration. Mechanistically, LINC01005 functioned as a competing endogenous RNA by sponging miR-128-3p, which in turn resulted in the upregulation of Krüppel-like factor 4 (KLF4). Inhibition of LINC01005 in the exosomes significantly abrogated the ox-LDL-induced VSMC phenotypic switch and the associated increase in cell proliferation and migration, while overexpression of miR-128-3p or silencing of KLF4 mitigated these effects. These findings elucidate a novel regulatory axis—the LINC01005/miR-128-3p/KLF4 pathway—underlying VSMC phenotypic modulation in the context of atherosclerosis (1)."}]}, {"type": "t", "text": "\n "}, {"type": "p", "children": [{"type": "fg", "children": [{"type": "fg_f", "ref": "1"}]}, {"type": "t", "text": ""}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Zhiliang Zhang, Dasong Yi, Jiamin Zhou, et al. "}, {"type": "b", "children": [{"type": "t", "text": "Exosomal LINC01005 derived from oxidized low-density lipoprotein-treated endothelial cells regulates vascular smooth muscle cell phenotypic switch."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Biofactors (2020)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1002/biof.1665"}], "href": "https://doi.org/10.1002/biof.1665"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "32663367"}], "href": "https://pubmed.ncbi.nlm.nih.gov/32663367"}]}]}]}