On October 9, the research team of Professor Chu Bo of the School of Basic Medical Sciences of Shandong University, together with the team of Professor Sun Jinpeng and Professor Yu Xiao, as well as the team of Professor Chai Renjie of Southeast University and Professor Xu Yunfei of Qilu Hospital of Shandong University, jointly published the latest research results "Sensing steroid hormone 17a-hydroxypregnenolone by GPR56 enables" online in the journal Cell Metabolism protection from ferroptosis-induced liver injury”. The research team identified the membrane receptor GPR56 of the steroid hormone 17a-hydroxypregnenolone as closely related to ferroptosis, and the study revealed for the first time that 17-OH PREG-GPR56-CD36 axis-mediated lipid metabolism is a new anti-ferroptosis pathway, and its mediated signal transduction is necessary for maintaining liver homeostasis, providing new drug research targets and therapeutic strategies for the development and application of therapeutics in clinical liver injury.

THE RESEARCH TEAM ELUCIDATED A NOVEL MOLECULAR MECHANISM BY WHICH THE STEROID METABOLITE 17-OH PREG RESISTS FERROPTOSIS VIA THE GPR56/ADGRG1 PATHWAY, AND REVEALED FOR THE FIRST TIME THE POTENTIAL IMPORTANT ROLE OF GPC-REGULATED FERROPTOSIS IN CLINICAL TREATMENT. The results of this study provide new insights into the potential treatment of liver injury, deeply dissect the close link between GPCR receptors and ferroptosis, and provide a new research strategy for the development and application of clinical treatment methods for ferroptosis-related diseases. This research was supported by the National Key R&D Program of China, the National Natural Science Foundation of China, the New Cornerstone Science Foundation and the National Science Foundation for Distinguished Young Scholars.