C1qtnf3, also known as C1q/TNF-related protein 3 (CTRP3), is a novel adipokine. It belongs to the C1q/TNF superfamily and has modulating effects on metabolism, inflammation, and the cardiovascular system [2,4]. It is involved in regulating glucose homeostasis, and can normalize blood glucose through several mechanisms [2].

In murine studies, C1qtnf3 was found to be an intra-ovarian factor promoting follicle growth. Its transcript abundance was higher in large follicles, and it was detected mainly in granulosa cells and oocytes of growing follicles. Excess androgen decreased its expression, while recombinant C1QTNF3 protein accelerated ovarian explant weight gain and pre-antral follicle growth induced by FSH in vitro, along with activation of the AKT/mTOR pathway [1].

In collagen-induced arthritis mouse models, C1qtnf3-deficient (C1qtnf3(-/-)) mice had a higher incidence and severity of arthritis, higher levels of antibodies against type II collagen and pro-inflammatory cytokine mRNAs compared to wild-type mice, indicating its important role in autoimmune arthritis development [3].

In conclusion, C1qtnf3 plays essential roles in multiple biological processes. In the ovary, it promotes folliculogenesis, and in the context of arthritis, it is involved in disease development. Gene-knockout mouse models have been crucial in revealing these functions, providing insights into potential therapeutic targets for related diseases such as infertility and rheumatoid arthritis.