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REVIEW

Cellular mechanisms of osteoporosis: A comprehensive perspective on ferroptosis, cuproptosis and lipid metabolism abnormalities

Hongfa Zhou1,2,3,4# ,  Jinhao Deng1,2,3,4# ,  Jingyuan Chen1,2,3,4 ,  Xuan Zhang1,2,3,4 ,  Liangbin Wu2,3,4 ,  Tiantian Qi2,3,4 ,  Hui Zeng5* ,  Kai Ren6* ,  Fei Yu6*
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1 Medical College, Shantou University, Shantou, Guangdong Province, China
2 Department of Bone & Joint Surgery, Peking University Shenzhen Hospital, Shenzhen, Guangdong Province, China
3 National & Local Joint Engineering Research Center of Orthopaedic Biomaterials, Shenzhen, Guangdong Province, China
4 Shenzhen Key Laboratory of Orthopaedic Diseases and Biomaterials Research, Shenzhen, Guangdong Province, China
5 Department of Orthopedics, Shenzhen Second People’s Hospital, The First Affiliated Hospital of Shenzhen University, Shenzhen, Guangdong Province, China
6 Department of Spine Surgery, Shenzhen Second People’s Hospital, The First Affiliated Hospital of Shenzhen University, Shenzhen, Guangdong Province, China
BMT, 78 https://doi.org/10.12336/bmt.24.00078
Submitted: 24 October 2024 | Revised: 31 December 2024 | Accepted: 15 May 2025 | Published: 17 December 2025
© 2025 by the Author(s). Licensee Biomaterials Translational, USA. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution-NonCommercial-ShareAlike 4.0 (CC BY-NC-SA 4.0) (https://creativecommons.org/licenses/by-nc-sa/4.0/deed.en)
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Abstract

Osteoporosis is a prevalent skeletal disorder characterised by reduced bone mineral density and compromised bone microarchitecture, leading to increased bone fragility and increased risk of fracture. Recent studies have implicated ferroptosis, cuproptosis, and dysregulated lipid metabolism as pivotal factors in the pathogenesis of osteoporosis. Ferroptosis is an iron-dependent form of cell death that disrupts the balance between osteoblast-mediated bone formation and osteoclast-mediated bone resorption by promoting lipid peroxidation and inducing cellular injury. Cuproptosis, associated with disruptions in copper homeostasis, influences bone cell integrity through oxidative stress and inflammatory responses, thereby impacting bone density. Aberrant lipid metabolism may exacerbate osteoporosis by disrupting bone-fat homeostasis, oxidative stress, and inflammatory responses. This review synthesizes the interplay between cuproptosis, ferroptosis, and lipid metabolism, elucidates the cellular mechanisms underlying osteoporosis, and accordingly provides novel therapeutic targets and intervention strategies, potentially enhancing osteoporosis prevention and treatment.

Keywords
Cuproptosis
Ferroptosis
Lipid metabolism
Osteoporosis
Oxidative stress
Funding
This work was supported by grants from National Natural Science Foundation of China (Nos. 82102568, 82172432), and Guangdong Basic and Applied Basic Research Foundation (Nos. 2022A1515220111, 2022B1515120046, 2021A1515220037, 2022A1515220165, 2021A1515110311, 2022A1515220055).
Conflict of interest
The authors declare that there is no conflict of interest.
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