C1ql4, also known as CTRP11, is a member of the C1q-and TNF-related protein family. It has diverse functions, being involved in processes like steroidogenesis, angiogenesis, and cell-adhesion regulation. In the context of signaling pathways, it activates the ERK1/2 signal pathway in angiogenesis [3]. It may also play a role in the PI3K/AKT/NF-κB signaling pathway in breast cancer [1].

In a Ctrp11-KO mouse model, male mice showed exacerbated obesity-induced glucose intolerance, suggesting a role for C1ql4 in systemic metabolism [5]. In the testis, C1ql4 knockdown in Leydig cells led to reduced Star expression, indicating its importance in steroidogenesis [2]. In myoblasts, secreted C1q-like1-4 proteins (including C1ql4) repress myoblast fusion by interacting with BAI3 [4].

In conclusion, C1ql4 is crucial in multiple biological processes. The gene knockout mouse models have revealed its role in metabolism-related diseases and reproductive processes. Its functions in angiogenesis and myoblast fusion also highlight its importance in tissue development and repair. These findings provide valuable insights into potential therapeutic targets for diseases related to these processes.