{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nVitronectin (VTN) is emerging as a central extracellular matrix component that regulates cell adhesion and differentiation. In multiple studies, VTN engagement alone or in complexes with growth factors has been shown to promote osteogenic differentiation of mesenchymal stem cells, enhance focal adhesion formation, and facilitate lineage‐specific outcomes such as oligodendrocyte maturation and keratinocyte migration in wound repair. These findings demonstrate that VTN not only serves as a physical substrate but also actively transduces cues that govern tissue repair and regeneration."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "5"}]}, {"type": "t", "text": ""}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nAt the molecular level, VTN functions as an integrative hub for cell–matrix interactions. It binds distinct integrin receptors and non‐integrin partners (e.g. urokinase receptor) to trigger both canonical and non‐canonical intracellular signaling pathways. Moreover, VTN is subject to proteolytic modifications – as demonstrated by cleavage by granzyme B and matrix metalloproteinase‐2 – which alter its adhesive properties and regulate downstream events such as inhibition of the complement membrane attack complex, modulation of platelet adhesion and clot stability, and even participation in receptor phosphorylation cascades. These studies also illustrate that pathogenic bacteria and viruses can subvert VTN interactions to anchor themselves to host cells."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "6", "end_ref": "17"}]}, {"type": "t", "text": ""}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond its roles in normal physiology, VTN is implicated in a range of pathological processes. In cancer, complexes containing VTN (often with IGFs, IGF‐binding proteins, or integrins) enhance tumor cell migration and invasion, while its altered serum concentration and glycosylation have been associated with conditions such as coronary artery disease, metabolic syndrome, and altered amyloid deposition. Similarly, several microbial pathogens—including Neisseria meningitidis, Haemophilus influenzae, Pseudomonas aeruginosa, and Candida species—exploit VTN to adhere to and invade host cells. Together, these studies underscore VTN’s multifaceted functions as an ECM adhesive molecule, a mediator of cell signaling, and a target for microbial and neoplastic subversion."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "18", "end_ref": "30"}]}, {"type": "t", "text": ""}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Roman M. Salasznyk, William A. Williams, Adele Boskey, et al. 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