C1QTNF1, also known as C1q And TNF Related 1, is a novel adipokine and a member of the C1q and TNF-related protein (CTRP) family. It has been shown to be involved in various biological processes.

In the cardiovascular system, it may play a role in regulating cardiac function through the AMPKa pathway [2]. In addition, it has been associated with lipid metabolism and inflammatory responses, potentially acting as a key mediator in integrating these processes in macrophages [3]. Genetic models such as knockout mouse models can be valuable for studying its functions.

In a study using C1QTNF1 knock-out mice, C1QTNF1 deficiency was found to accelerate cardiac hypertrophy, fibrosis, inflammation responses, and oxidative stress with deteriorating cardiac dysfunction in the Ang II-induced cardiac hypertrophy mouse model. This indicates that C1QTNF1 is a negative regulator of cardiomyocyte hypertrophy, and its anti-hypertrophic effects rely on AMPKa activation [2]. In kidney renal clear cell carcinoma (KIRC), knockdown of C1QTNF1 inhibited cell proliferation, migration, and invasion, suggesting that high C1QTNF1 expression is associated with KIRC progression [1].

In conclusion, C1QTNF1 has diverse biological functions. Its role in cardiac hypertrophy and fibrosis is significant, as it can improve cardiac function by activating the AMPKa pathway. In KIRC, C1QTNF1 is related to tumor progression. The study of C1QTNF1 using knockout mouse models provides important insights into its functions in these specific disease areas, helping to understand the underlying biological mechanisms and potentially providing new targets for treatment.