Wu Heng, Zuo Junhui, Dai Yu, Li Hairui, Wang Song
Department of Orthopedics, the Affiliated Hospital of Southwest Medical University, Luzhou, 646000, China.
Department of Oncology, the Affiliated Hospital of Southwest Medical University, Luzhou, 646000, China.
J Orthop Surg Res. 2025 Jan 24;20(1):92. doi: 10.1186/s13018-025-05517-5.
Osteoporosis is a systemic skeletal disorder characterized by reduced bone density and an increased risk of fractures, particularly prevalent in the aging population. Osteoporotic complications, including vertebral compression fractures, hip fractures, and distal forearm fractures, affect over 8.9 million individuals globally, placing a significant economic strain on healthcare systems. Recent advances have expanded our understanding of the mechanisms underlying osteoporosis, particularly the intricate regulatory networks involved in bone metabolism. A central player in these processes is ubiquitin-mediated proteasomal degradation, a crucial post-translational modification system that involves ubiquitin, the ubiquitin-activating enzyme (E1), ubiquitin-conjugating enzyme (E2), ubiquitin ligase (E3), deubiquitinating enzymes, and the proteasome. Among the various E3 ligases, the NEDD4 family has emerged as a key regulator of both bone development and osteoporotic pathology. This review delineates the role of NEDD4 family in osteoporosis and identifies potential drug targets within these pathways, offering insights into novel therapeutic approaches for osteoporosis through targeted intervention.
骨质疏松症是一种全身性骨骼疾病,其特征是骨密度降低和骨折风险增加,在老年人群中尤为普遍。骨质疏松症并发症,包括椎体压缩性骨折、髋部骨折和远端前臂骨折,全球有超过890万人受其影响,给医疗系统带来了巨大的经济压力。最近的进展拓宽了我们对骨质疏松症潜在机制的理解,尤其是参与骨代谢的复杂调控网络。这些过程中的一个核心因素是泛素介导的蛋白酶体降解,这是一种关键的翻译后修饰系统,涉及泛素、泛素激活酶(E1)、泛素结合酶(E2)、泛素连接酶(E3)、去泛素化酶和蛋白酶体。在各种E3连接酶中,NEDD4家族已成为骨骼发育和骨质疏松症病理的关键调节因子。这篇综述阐述了NEDD4家族在骨质疏松症中的作用,并确定了这些途径中的潜在药物靶点,通过靶向干预为骨质疏松症的新型治疗方法提供了见解。