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骨代谢——一个未得到充分重视的因素。

Bone metabolism - an underappreciated player.

作者信息

Choi In Ah, Umemoto Akio, Mizuno Masataka, Park-Min Kyung-Hyun

机构信息

Arthritis and Tissue Degeneration Program, David Z. Rosensweig Genomics Research Center, Hospital for Special Surgery, New York, NY, 10021, USA.

Department of Internal Medicine, College of Medicine, Chungbuk National University, Cheongju, Chungcheongbuk-do, 28644, Republic of Korea.

出版信息

NPJ Metab Health Dis. 2024 Jul 1;2(1):12. doi: 10.1038/s44324-024-00010-9.


DOI:10.1038/s44324-024-00010-9
PMID:40604262
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12118745/
Abstract

Bone is constantly being remodeled, and this process is orchestrated by a dynamic crosstalk of bone cells, including osteoclasts, osteoblasts, and osteocytes. Recent evidence suggests that cellular metabolism plays a crucial role in the differentiation and function of bone cells and facilitates the adaptation of bone cells to changes in the bone microenvironment. Moreover, bone affects whole-body energy metabolism. However, it is not yet completely understood how different cells in bone coordinate metabolic processes under physiological conditions, and how altered metabolic processes in bone cells contribute to pathological conditions where the balance among bone cells is disrupted. Therefore, gaining a better understanding of the distinct metabolic requirements of bone cells can provide crucial insights into the dysfunction of bone cells in pathological conditions and can be used to identify new therapeutic approaches to treat bone diseases. Here, we discuss recent advances in understanding metabolic reprogramming in bone cells.

摘要

骨骼不断进行重塑,这一过程由包括破骨细胞、成骨细胞和骨细胞在内的骨细胞动态相互作用精心编排。最近的证据表明,细胞代谢在骨细胞的分化和功能中起关键作用,并促进骨细胞适应骨微环境的变化。此外,骨骼会影响全身能量代谢。然而,目前尚未完全了解骨骼中的不同细胞在生理条件下如何协调代谢过程,以及骨细胞中改变的代谢过程如何导致骨细胞平衡被破坏的病理状况。因此,更好地了解骨细胞独特的代谢需求可以为病理状况下骨细胞的功能障碍提供关键见解,并可用于确定治疗骨疾病的新治疗方法。在此,我们讨论在理解骨细胞代谢重编程方面的最新进展。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8654/12118745/934f0fde571b/44324_2024_10_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8654/12118745/bb250b23cd82/44324_2024_10_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8654/12118745/391283793979/44324_2024_10_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8654/12118745/934f0fde571b/44324_2024_10_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8654/12118745/bb250b23cd82/44324_2024_10_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8654/12118745/391283793979/44324_2024_10_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8654/12118745/934f0fde571b/44324_2024_10_Fig3_HTML.jpg

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本文引用的文献

[1]
Lactate-induced histone lactylation by p300 promotes osteoblast differentiation.

PLoS One. 2023

[2]
Lipolysis supports bone formation by providing osteoblasts with endogenous fatty acid substrates to maintain bioenergetic status.

Bone Res. 2023-11-24

[3]
Mitigation of Osteoclast-Mediated Arthritic Bone Remodeling By Short Chain Fatty Acids.

Arthritis Rheumatol. 2024-4

[4]
Sexual dimorphism of osteoclast reliance on mitochondrial oxidation of energy substrates in the mouse.

JCI Insight. 2023-12-22

[5]
L-arginine metabolism inhibits arthritis and inflammatory bone loss.

Ann Rheum Dis. 2024-1-2

[6]
Arginine methylation of PPP1CA by CARM1 regulates glucose metabolism and affects osteogenic differentiation and osteoclastic differentiation.

Clin Transl Med. 2023-9

[7]
Effects of PTH on osteoblast bioenergetics in response to glucose.

Bone Rep. 2023-7-24

[8]
Origin of Osteoclasts: Osteoclast Precursor Cells.

J Bone Metab. 2023-5

[9]
Oxidative phosphorylation in bone cells.

Bone Rep. 2023-5-23

[10]
Responses to Vitamin D Supplementation in Individuals With Overweight and Obesity.

JAMA Netw Open. 2023-1-3

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