GDF7 (growth differentiation factor 7) is a member of the TGF-β protein superfamily that functions as a secreted cytokine involved in cellular differentiation, tissue repair, and disease pathogenesis 1. The protein acts through BMP signaling pathways, specifically binding to BMP receptors (BMPR1A, BMPR2) to activate SMAD-dependent signaling cascades 23. In physiological contexts, GDF7 promotes osteogenic differentiation of human adipose-derived stem cells via AKT and p38 signaling pathways 1 and supports hepatic progenitor cell expansion during liver repair 2. However, dysregulated GDF7 expression contributes to several pathological conditions. In glaucoma, TET-dependent GDF7 hypomethylation leads to excessive protein production, promoting trabecular meshwork fibrosis through BMPR2/Smad signaling and creating aqueous humor outflow resistance 3. GDF7 is also upregulated in enamel renal syndrome, contributing to intrapulpal calcifications through enhanced BMP signaling 4. Clinically, GDF7 variants are associated with Barrett's esophagus and esophageal adenocarcinoma risk 5, while GDF7 expression patterns serve as prognostic indicators in prostate cancer 6 and intrauterine adhesions 7. These findings establish GDF7 as both a tissue repair mediator and potential therapeutic target for fibrotic diseases.