Gper1, also known as GPR30, is a G protein-coupled estrogen receptor. It binds 17-β-estradiol (E2) and is involved in non-genomic estrogen signaling, regulating various biological processes. It has been associated with multiple pathways such as kinase cascades, calcium flux, and may crosstalk with classical estrogen receptors [3,4].

In multiple myeloma, GPER1 mRNA is down-regulated in plasma cells from patients, and lower expression associates with worse overall survival. Pharmacological activation of GPER1 using G-1 shows anti-MM activity through apoptosis induction and overcomes the protective effects of bone marrow stromal cells [1].

In the UUO-induced renal fibrosis model, activation of GPER1 in macrophages reduces renal fibrotic lesions and macrophage infiltration, while Gper1 deletion in male mice accelerates renal fibrosis [2].

In osteoblast precursors, T3-induced osteogenesis is mediated by GPER1-regulated glycolysis [5].

In hippocampal function, GPER1 deficiency in mice causes sex-specific dysregulation of plasticity and cognitive function, with males showing reduced anxiety and females showing increased fear response and impaired spatial learning [6].

In conclusion, Gper1 plays crucial roles in multiple biological processes and disease conditions. Model-based research, especially gene knockout studies in mice, has revealed its significance in cancer, renal fibrosis, osteogenesis, and cognitive function. Understanding Gper1 can potentially provide new therapeutic targets for related diseases.