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Review

The role of autophagy/lipophagy in the response of osteoblastic cells to hyperlipidemia (Review)

  • Authors:
    • Yizhang He
    • Yantong Liu
    • Ran Li
    • Aoqi Xiang
    • Xiaochang Chen
    • Qi Yu
    • Peihong Su
  • View Affiliations / Copyright

    Affiliations: Shaanxi Provincial Key Laboratory of Ischemic Cardiovascular Disease, Institute of Basic and Translational Medicine, Xi'an Medical University, Xi'an, Shaanxi 710021, P.R. China, School of Basic Medical Sciences, Xi'an Medical University, Xi'an, Shaanxi 710021, P.R. China
  • Article Number: 328
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    Published online on: June 19, 2024
       https://doi.org/10.3892/etm.2024.12617
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Abstract

There has been interest in the connection between cardiovascular diseases and osteoporosis, both of which share hyperlipidemia as a common pathological basis. Osteoporosis is a progressive metabolic bone disease characterized by reduced bone mass, deteriorated bone microstructure, increased bone fragility and heightened risk of bone fractures. Dysfunction of osteoblastic cells, vital for bone formation, is induced by excessive internalization of lipids under hyperlipidemic conditions, forming the crux of hyperlipidemia‑associated osteoporosis. Autophagy, a process fundamental to cell self‑regulation, serves a critical role in osteoblastic cell function and bone formation. When activated by lipids, lipophagy inhibits osteoblastic cell differentiation in response to elevated lipid concentrations, resulting in reduced bone mass and osteoporosis. However, an in‑depth understanding of the precise roles and mechanisms of lipophagy in the regulation of osteoblastic cell function is required. Study of the molecular mechanisms governing osteoblastic cell response to excessive lipids can result in a clearer understanding of osteoporosis; therefore, potential strategies for preventing hyperlipidemia‑induced osteoporosis can be developed. The present review discusses recent progress in elucidating the molecular mechanisms of lipophagy in the regulation of osteoblastic cell function, offering insights into hyperlipidemia‑induced osteoporosis.
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Copy and paste a formatted citation
Spandidos Publications style
He Y, Liu Y, Li R, Xiang A, Chen X, Yu Q and Su P: The role of autophagy/lipophagy in the response of osteoblastic cells to hyperlipidemia (Review). Exp Ther Med 28: 328, 2024.
APA
He, Y., Liu, Y., Li, R., Xiang, A., Chen, X., Yu, Q., & Su, P. (2024). The role of autophagy/lipophagy in the response of osteoblastic cells to hyperlipidemia (Review). Experimental and Therapeutic Medicine, 28, 328. https://doi.org/10.3892/etm.2024.12617
MLA
He, Y., Liu, Y., Li, R., Xiang, A., Chen, X., Yu, Q., Su, P."The role of autophagy/lipophagy in the response of osteoblastic cells to hyperlipidemia (Review)". Experimental and Therapeutic Medicine 28.2 (2024): 328.
Chicago
He, Y., Liu, Y., Li, R., Xiang, A., Chen, X., Yu, Q., Su, P."The role of autophagy/lipophagy in the response of osteoblastic cells to hyperlipidemia (Review)". Experimental and Therapeutic Medicine 28, no. 2 (2024): 328. https://doi.org/10.3892/etm.2024.12617
Copy and paste a formatted citation
x
Spandidos Publications style
He Y, Liu Y, Li R, Xiang A, Chen X, Yu Q and Su P: The role of autophagy/lipophagy in the response of osteoblastic cells to hyperlipidemia (Review). Exp Ther Med 28: 328, 2024.
APA
He, Y., Liu, Y., Li, R., Xiang, A., Chen, X., Yu, Q., & Su, P. (2024). The role of autophagy/lipophagy in the response of osteoblastic cells to hyperlipidemia (Review). Experimental and Therapeutic Medicine, 28, 328. https://doi.org/10.3892/etm.2024.12617
MLA
He, Y., Liu, Y., Li, R., Xiang, A., Chen, X., Yu, Q., Su, P."The role of autophagy/lipophagy in the response of osteoblastic cells to hyperlipidemia (Review)". Experimental and Therapeutic Medicine 28.2 (2024): 328.
Chicago
He, Y., Liu, Y., Li, R., Xiang, A., Chen, X., Yu, Q., Su, P."The role of autophagy/lipophagy in the response of osteoblastic cells to hyperlipidemia (Review)". Experimental and Therapeutic Medicine 28, no. 2 (2024): 328. https://doi.org/10.3892/etm.2024.12617
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