Abstract:Growth differentiation factor 10 (GDF10) is an atypical member of the transforming growth factor-β/bone morphogenetic protein (TGF-β/BMP) family, which has recently been proposed to participate in osteogenic-like transdifferentiation of vascular smooth muscle cell (VSMC) and vascular calcification. Within the primary signaling networks governing osteoblastic-like transdifferentiation of VSMC and vascular calcification, this article systematically summarizes in vivo, in vitro, and clinical evidence for GDF10's role in bone, cardiovascular system, and vascular calcification, and compares GDF10 with other TGF-β/BMP ligands according to their receptor Smad signaling profiles. Experimental studies indicate that GDF10 generally exhibits an inhibitory effect on osteogenesis in bone-related models. In vascular calcification, single-cell analysis of atherosclerotic plaques has linked GDF10 to the enrichment of osteogenic-like VSMC and plaque instability; By contrast, medial calcification models induced by hyperphosphatemia or chronic kidney disease (CKD) demonstrate that recombinant GDF10 downregulates Runx2 and alleviates calcification. In summary, GDF10 may exert context-dependent, bidirectional effects on vascular calcification. On this basis, this article proposes an environment-dependent regulatory hypothesis and preliminarily discusses its potential value as a biomarker and therapeutic target.Further mechanistic and clinical studies are still required for validation.
