{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nVEGF‐B is an enigmatic member of the vascular endothelial growth factor family that exists in multiple isoforms and engages primarily with VEGF receptor‐1 and the neuropilin‐1 coreceptor. Structural studies have revealed that VEGF‐B adopts a cysteine‐knot motif that, although similar to that of VEGF‐A and placental growth factor, displays unique receptor‐binding determinants that likely contribute to its tissue‐selective actions. Notably, VEGF‐B is expressed in peripheral tissues such as the skin—where fibroblasts produce detectable levels with distinct regulatory patterns—further supporting its context‐dependent roles. Its endogenous function in pathological angiogenesis, however, remains ambiguous."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "6"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn cardiovascular and metabolic contexts, experimental models have illuminated critical roles for VEGF‐B in modulating lipid metabolism and tissue remodeling. Cardiac‐specific overexpression of VEGF‐B in mice has been shown to induce concentric myocardial hypertrophy accompanied by distinct shifts in lipid profiles and mitochondrial integrity, while elevated VEGF‐B in diabetic kidney disease models correlates with renal lipotoxicity and insulin resistance. Moreover, clinical investigations have linked circulating VEGF‐B levels to dyslipidemia and target‐organ damage, underscoring its potential as a therapeutic target in metabolic disorders and cardiovascular injury."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "7", "end_ref": "12"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn the realm of tumor biology and inflammatory regulation, VEGF‐B exhibits a multifaceted, context‐dependent influence on neovascularization and cancer progression. Its expression—detected in immune cells such as basophils—suggests that VEGF‐B may contribute to inflammatory processes. In several malignancies, including hepatocellular, colorectal, and gastric cancers, aberrant or co‐expressed VEGF‐B with its receptors has been associated with enhanced angiogenic signaling, increased extracellular protease activity, and ultimately greater invasive behavior and metastatic potential. Intriguingly, under conditions characterized by high FGF2/FGFR1 expression, VEGF‐B has been reported to act as an endogenous inhibitor of angiogenesis, highlighting a dual regulatory role that may depend on the local balance of growth‐factor signals. In disorders as diverse as polycystic ovary syndrome, these alterations in VEGF‐B expression further support its involvement in modulating disease pathology."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "13", "end_ref": "24"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond its vascular and metabolic roles, VEGF‐B also appears to exert neuroprotective and neurotrophic effects. Elevated expression in dysplastic neurons and in models of amyotrophic lateral sclerosis suggests that VEGF‐B may promote neuronal survival via autocrine and paracrine signaling mechanisms. In ocular tissues, VEGF‐B contributes to pathological neovascularization linked with diabetic retinopathy, while circulating levels have also been associated with modifications in insulin secretion dynamics—underscoring an intersection between neurovascular integrity and metabolic control. Additionally, novel peptide‐based strategies targeting the VEGF‐B/neuropilin‐1 axis are under investigation, pointing to promising therapeutic applications in neurologic and inflammatory conditions."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "25", "end_ref": "31"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Maija Bry, Riikka Kivelä, Veli-Matti Leppänen, et al. 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