| Bone metabolic diseases refer to conditions in which an imbalance between bone resorption and bone formation leads to decreased bone density and bone quality, resulting in abnormalities in the skeletal system. Common bone metabolic diseases include osteoporosis, bone defects, fractures and nonunion, femoral head necrosis, Paget's disease, and others. The occurrence of these diseases is often associated with imbalances between osteoblast and osteoclast function, abnormal hormone levels, and metabolic disorders. Molecules like HIF-1α play an important regulatory role. HIF-1α is activated in hypoxic environments and regulates bone resorption by regulating cell metabolism, promoting proliferation and differentiation of osteoblasts while inhibiting formation of osteoclasts. It also regulates bone metabolism by controlling bone angiogenesis, as well as the proliferation, migration, and osteogenic differentiation of bone marrow mesenchymal stem cells. HIF-1α is regulated by various factors, including hypoxia, energy metabolism, cofactor activity, non-coding RNAs, trace elements, and others. As a key pathway coupling angiogenesis and osteogenesis, HIF-1α has been widely studied in the context of bone metabolic diseases such as bone defects, osteoporosis, femoral head necrosis, fractures, and nonunion. This paper explores in depth the regulatory role of the HIF-1α pathway in bone homeostasis and angiogenesis, its mechanisms, and highlights the latest experimental research on the application of HIF-1α in bone metabolic diseases. |