| Description | Decreased m6A level in bone marrow mesenchymal stem cells (MSCs) induces pathological features of osteoporosis in mice (impaired bone formation, incompetent osteogenic differentiation potential, and increased marrow adiposity). PTH (parathyroid hormone)/Pth1r (parathyroid hormone receptor-1) signaling axis is an important downstream pathway for m6A regulation in MSCs. METTL3 loss of function reduces the translation efficiency of MSCs lineage allocator Pth1r and disrupts the PTH-induced osteogenic and adipogenic responses in vivo. |