C1qtnf3, also known as C1q/Tumor Necrosis Factor-related protein 3 (CTRP3), is a member of the C1q/TNF superfamily. It is a novel adipokine expressed in various tissues like adipose tissue, ovary, etc. C1qtnf3 is involved in multiple biological processes such as metabolism, inflammation, and cell growth regulation. It can modulate cytokine and adipokine expression, and is related to glucose homeostasis and immune-related pathways [2,4].

In the murine ovary, C1qtnf3 promotes follicle growth by accelerating granulosa cell proliferation, decelerating apoptosis, and promoting AKT/mTOR phosphorylation. Intrabursal administration of the C1QTNF3 antibody in vivo delayed gonadotropin-induced antral follicle development, indicating its role in folliculogenesis [1]. In collagen-induced arthritis mouse models, C1qtnf3 knockout (C1qtnf3 -/-) mice had a higher incidence and severity of arthritis, with higher levels of antibodies against type II collagen and pro-inflammatory cytokine mRNAs compared to wild-type mice, suggesting its importance in the development of autoimmune arthritis [3].

In conclusion, C1qtnf3 is a multi-functional adipokine involved in processes like folliculogenesis and regulation of autoimmune arthritis. The use of gene knockout mouse models has been crucial in revealing its role in these specific biological processes and disease conditions, providing insights into potential therapeutic targets for ovarian-related disorders and rheumatoid arthritis.