{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nThe very‐low‐density lipoprotein receptor (VLDLR) is a multifunctional member of the low‐density lipoprotein receptor family with a central role in lipid homeostasis. VLDLR binds various forms of apolipoprotein E–containing lipoproteins and is regulated by factors such as PCSK9, which targets it for degradation. Such regulation affects cholesterol uptake and clearance in both lipid‐rich and lipid‐poor environments, thereby contributing to the control of plasma low‐density lipoprotein levels and even impacting pathological lipid accumulation as observed in certain renal carcinomas."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "4"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn addition to its metabolic role, VLDLR is critical for normal brain development via its participation in reelin signaling. By binding reelin, VLDLR (in concert with ApoER2) initiates a cascade leading to phosphorylation of intracellular adaptors that guide neuronal migration and proper lamination of the cerebral cortex and cerebellum. Mutations or deletions that affect VLDLR cause severe neurodevelopmental disorders—including cerebellar hypoplasia, dysequilibrium syndrome, and even quadrupedal locomotion—and altered receptor expression has been investigated as a peripheral marker in neuropsychiatric conditions such as schizophrenia."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "5", "end_ref": "12"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nVLDLR also influences ocular health by acting as a negative regulator of pathological neovascularization. In the retina, loss of VLDLR activity is associated with up‐regulation of vascular endothelial growth factor (VEGF) and activation of the Wnt/β‐catenin pathway, processes that contribute to subretinal neovascularization as seen in wet age‐related macular degeneration (AMD)."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "13", "end_ref": "15"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nVLDLR further functions as an alternative receptor in host–pathogen interactions and in neurobehavioral regulation. It facilitates the entry of certain viruses, including minor‐group human rhinoviruses and hepatitis C virus, particularly under hypoxic conditions, independently of canonical receptors. Moreover, genetic association studies have linked VLDLR variants with behavioral traits such as disordered gambling, and experimental work indicates that VLDLR modulates dendritic cell–dependent adaptive immune responses in allergic airway inflammation."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "16", "end_ref": "19"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn cancer biology, aberrant VLDLR expression has been observed in diverse malignancies such as gastric, breast, lung, and colorectal cancers. Changes in VLDLR levels—as mediated by microRNAs including miR-135a-5p and miR-200c—affect tumor cell proliferation and migration, suggesting that beyond its role in lipid uptake, VLDLR influences key signaling pathways that contribute to tumorigenesis."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "20", "end_ref": "22"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nAt the molecular level, VLDLR undergoes regulated proteolytic processing and intracellular trafficking that fine-tune its signaling capability. Ligand binding triggers extracellular cleavages and intramembranous proteolysis, processes that generate distinct receptor fragments involved in downstream signal transduction. In parallel, quality control mechanisms in the endoplasmic reticulum—including chaperone interactions and proteasomal degradation—ensure proper receptor folding and turnover, thereby modulating its interactions with ligands such as coagulation factor VIII."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "23", "end_ref": "28"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nFinally, transcriptional regulation and broader vascular responses further expand the physiological impact of VLDLR. Transcriptional repressors such as HIC1 have been shown to down-regulate VLDLR, influencing not only neural and mammary epithelial development but also vascular functions including macrophage-mediated cholesterol efflux and responses to triglyceride-rich lipoproteins. 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