Lipid metabolic networks in osteoarthritis pathogenesis: from sys-temic regulation to intrinsic control in chondrocytes
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Yan ZHAO1, Zitong DING1, Yan XUE2, Ziyuan YANG1, Jianan ZHANG3, Mengjie WU1. Lipid metabolic networks in osteoarthritis pathogenesis: from sys-temic regulation to intrinsic control in chondrocytes[J]. Journal of Zhejiang University Science B, 1998, -1(-1): .
@article{title="Lipid metabolic networks in osteoarthritis pathogenesis: from sys-temic regulation to intrinsic control in chondrocytes",
author="Yan ZHAO1, Zitong DING1, Yan XUE2, Ziyuan YANG1, Jianan ZHANG3, Mengjie WU1",
journal="Journal of Zhejiang University Science B",
volume="-1",
number="-1",
pages="",
year="1998",
publisher="Zhejiang University Press & Springer",
doi="10.1631/jzus.B2600231"
}
%0 Journal Article
%T Lipid metabolic networks in osteoarthritis pathogenesis: from sys-temic regulation to intrinsic control in chondrocytes
%A Yan ZHAO1
%A Zitong DING1
%A Yan XUE2
%A Ziyuan YANG1
%A Jianan ZHANG3
%A Mengjie WU1
%J Journal of Zhejiang University SCIENCE B
%V -1
%N -1
%P
%@ 1673-1581
%D 1998
%I Zhejiang University Press & Springer
%DOI 10.1631/jzus.B2600231
TY - JOUR
T1 - Lipid metabolic networks in osteoarthritis pathogenesis: from sys-temic regulation to intrinsic control in chondrocytes
A1 - Yan ZHAO1
A1 - Zitong DING1
A1 - Yan XUE2
A1 - Ziyuan YANG1
A1 - Jianan ZHANG3
A1 - Mengjie WU1
J0 - Journal of Zhejiang University Science B
VL - -1
IS - -1
SP -
EP - 0
%@ 1673-1581
Y1 - 1998
PB - Zhejiang University Press & Springer
ER -
DOI - 10.1631/jzus.B2600231
Abstract: Osteoarthritis (OA) is a leading cause of chronic joint degeneration, and recent research increasingly highlights the pivotal role of lipid metabolism in its development. This review offers a comprehensive analysis of how systemic lipid metabolic dysfunction, local joint tissue remodeling, and intracellular lipid regulation in chondrocytes contribute to OA progression. We examine how obesity, dietary patterns, and gut microbiota imbalances promote systemic lipid disturbances, which, in turn, drive chronic inflammation and cartilage degradation. At the joint level, disrupted lipid metabolism in the infrapatellar fat pad (IPFP), synovial tissue, and macrophages creates a pro-inflammatory environment that accelerates cartilage damage. Additionally, alterations in intracellular lipid homeostasis in chondrocytes are linked to oxidative stress, mitochondrial dysfunction, and ferroptosis, which further contribute to cell death and joint destruction. This review presents an integrated framework that connects these multi-level lipid metabolic disturbances, emphasizing their combined effects on OA progression. It also explores emerging therapeutic strategies targeting lipid metabolic pathways at the systemic, local, and cellular levels. The findings provide a solid theoretical foundation for the development of precision therapies focused on lipid metabolism modulation, offering new possibilities for OA management and potential intervention.
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