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Complement C1q and tumor necrosis factor-related protein 9B (C1QTNF9B, CTRP9B) is an adipokine and secretory glycoprotein closely related to adiponectin, and is involved in the regulation of glucose and lipid metabolism, vasodilation, cell differentiation, and suppression of inflammation[1][2]. It is produced intracellularly, but can form heterotrimers with its paralog CTRP9A, enabling robust secretion. CTRP9B activates key metabolic and anti-inflammatory signaling pathways, such as AMPK, AKT, and MAPK. It plays significant protective roles in cardiovascular diseases (including atherosclerosis and myocardial injury), diabetes, and pulmonary hypertension. CTRP9B is explored as a potential biomarker and therapeutic target due to its pleiotropic effects in metabolic and inflammatory conditions. Ongoing basic and translational research is investigating its broader physiological roles and therapeutic potential[1][2][4].
Activation of AMPK (adenosine monophosphate-activated protein kinase), AKT serine/threonine kinase, and eNOS (endothelial nitric oxide synthase) pathways to regulate metabolism, promote vasodilation, and suppress inflammation
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