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Complement C1q tumor necrosis factor-related protein 7 (C1QTNF7, also known as CTRP7) is a secreted glycoprotein belonging to the C1q/TNF-related protein (CTRP) family, which shares structural features with both complement C1q and the tumor necrosis factor ligand superfamily[1][2][3]. This protein is characterized by a collagen-like stalk and a globular C1q domain that allows trimerization and higher order oligomerization, often forming part of a collagen trimer structure[1][4].\nC1QTNF7 is implicated in a broad range of biological activities, including metabolic regulation (with increased circulating levels found in obesity, insulin resistance, and metabolic syndrome), modulation of immune and inflammatory responses, and potential neural or behavioral roles as indicated by genetic associations with conduct disorder and altered expression in neurodegenerative disease[2][3][5].\nRecent evidence also highlights C1QTNF7 as a host factor necessary for SARS-CoV-2 replication, suggesting a role in infectious disease biology[2]. In humans, its expression is highly regulated in metabolic tissues (such as adipose tissue), neural tissues, and in response to metabolic and immune system perturbations[5].\nLike other CTRPs, the receptors and downstream signaling pathways for C1QTNF7 remain incompletely defined; AdipoR1 has been implicated as a receptor for some family members, but direct evidence for C1QTNF7-specific receptors is currently lacking[1].\nDue to these pleiotropic functions, C1QTNF7 is considered a potential therapeutic target and biomarker—particularly in metabolic and inflammatory diseases, neurodegeneration, and infection—but no drug interactions or clinical inhibitors are currently known[1][2][3].
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