REVIEW article
Front. Cell Dev. Biol.
Sec. Cell Growth and Division
Volume 13 - 2025 | doi: 10.3389/fcell.2025.1602240
SNX10 in Autosomal Recessive Osteosclerosis, Osteosarcoma, Rheumatoid Arthritis, and Osteoporosis: Molecular Mechanisms and Therapeutic Implications
Provisionally accepted
- 1Chengdu University of Traditional Chinese Medicine, Chengdu, Sichuan Province, China
- 2First Affiliated Hospital of Xiamen University, Xiamen, Fujian Province, China
- 3China Three Gorges University, Hubei, China
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Bone metabolic diseases are typically caused by abnormal cell metabolism and cell death within the bone, involving cell types such as osteoblasts, osteoclasts, osteocytes, chondrocytes, and bone marrow mesenchymal stem cells. Bone metabolic diseases include autosomal recessive osteosclerosis (ARO), osteosarcoma (OS), rheumatoid arthritis (RA), and osteoporosis (OP). However, there are other categories of bone metabolic disorders in addition to the four mentioned in this review, including, but not limited to, osteochondrosis, Paget's disease, and hyperparathyroidism-associated bone disease, and others. The incidence of bone metabolism-related diseases has gradually increased over time and social changes, affecting a wider and wider group of people. Therefore, systematically analyzing the molecular pathological mechanisms of bone metabolic diseases, particularly the spatiotemporal dynamics of key regulatory nodes, has become an urgent need for developing novel therapeutic strategies. It is important to note that strictly speaking OS and RA are not usually categorized as bone metabolic disorders. However, this review categorizes them as bone metabolic diseases because of the pathological mechanisms, cellular metabolic abnormalities, and clinical evidence explored in OS and RA. Both OS and RA fit the basic profile of bone metabolic diseases. SNX10, as a member of the sorting nexin family, exerts unique regulatory functions in membrane transport through its phospholipid-binding properties mediated by the PX (phox homology) domain.Recent mechanistic analyses have shown that SNX10 exhibits multidimensional therapeutic potential in bone metabolic diseases by regulating pathways such as vesicle transport, lysosome maturation, and RANKL signal transduction. This review systematically integrates the latest research evidence on SNX10 in bone metabolic diseases, focusing on elucidating its molecular regulatory networks in conditions such as ARO, OS, RA, and OP, aiming to provide a theoretical basis for the application of SNX10-targeted precision therapeutic strategies in bone metabolic diseases.
Keywords: SNX10, autosomal recessive osteosclerosis, Osteosarcoma, Rheumatoid arthritis, Osteoporosis
Received: 31 Mar 2025; Accepted: 02 Jun 2025.
Copyright: © 2025 Liu, Deng, Liu, Zhang, Chen, Zhou and Zheng. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence: Chengqiang Zheng, Chengdu University of Traditional Chinese Medicine, Chengdu, 610075, Sichuan Province, China
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