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C1qtnf9, also known as CTRP9 (C1q-tumor necrosis factor-related protein-9), is involved in multiple biological processes. It has been associated with pathways such as the ERK5-GATA4 pro-hypertrophic pathway, AMPK-Nrf2 signaling, and TLR4/MD2/MyD88 and AMPK-NF-κB pathways [2,4,5]. It plays an important role in heart remodeling, immune microenvironment regulation, and metabolic processes [1,2,7]. Genetic models, especially mouse models, have been crucial in studying its functions.

In mouse models, C1qtnf9 knockout mice were protected from the development of cardiac hypertrophy, left ventricular dilatation, and dysfunction during transverse aortic constriction (TAC). This indicates that C1qtnf9 promotes maladaptive cardiac remodeling and left ventricular dysfunction [2]. In a study on myocardial infarction in rats, CTRP9 alleviated inflammation by activating Nrf2 [3]. In an in vitro model of pregnancy-induced hypertension, CTRP9 protected human placental vascular endothelial cells from hypoxia/reoxygenation-mediated injuries through activating AMPK/Nrf2 signaling [4]. Also, in rats with hypoxia-induced pulmonary hypertension, CTRP9 overexpression ameliorated the condition by regulating the secretion of endothelin-1 and nitric oxide mediated by AMPK [6].

In conclusion, C1qtnf9 is involved in various biological functions, especially in the cardiovascular system and metabolic regulation. Gene knockout mouse models have been instrumental in revealing its role in cardiac hypertrophy, heart failure, and other cardiovascular-related diseases, providing potential therapeutic targets for these conditions [2].