Inhibition of Toll-Like Receptor 3 Relieves Osteoarthritis by Suppression of Cartilage Degradation, Nuclear Factor Kappa B–Mediated Inflammation, and Activation of Autophagy

TLR3 drives OA progression through dual mechanisms: 1. Pro-inflammatory Pathway: Activates NF-κB signaling to amplify cytokine release and cartilage matrix breakdown. 2. Autophagy Suppression: Inhibits autophagy-related proteins, impairing cellular homeostasis. Targeting TLR3 may represent a therapeutic strategy to balance inflammation and autophagy, potentially slowing OA progression in multi-joint involvement cases.

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Publication Details

Journal
Cartilage
Published
2025-06-24
DOI
https://doi.org/10.1177/19476035251317713
Citations
1
Primary Topic
Osteoarthritis Treatment and Mechanisms
Type
article
Field-Weighted Citation Impact
1.67
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article

Inhibition of Toll-Like Receptor 3 Relieves Osteoarthritis by Suppression of Cartilage Degradation, Nuclear Factor Kappa B–Mediated Inflammation, and Activation of Autophagy

Shun Cao, Zhe Hou, Mou Wang
1 citations
Cartilage
Osteoarthritis Treatment and Mechanisms
1.67
article

Inhibition of Toll-Like Receptor 3 Relieves Osteoarthritis by Suppression of Cartilage Degradation, Nuclear Factor Kappa B–Mediated Inflammation, and Activation of Autophagy

Shun Cao, Zhe Hou, Mou Wang
article en
1 citations

Abstract

TLR3 drives OA progression through dual mechanisms: 1. Pro-inflammatory Pathway: Activates NF-κB signaling to amplify cytokine release and cartilage matrix breakdown. 2. Autophagy Suppression: Inhibits autophagy-related proteins, impairing cellular homeostasis. Targeting TLR3 may represent a therapeutic strategy to balance inflammation and autophagy, potentially slowing OA progression in multi-joint involvement cases.

Cartilage
Nanjing University of Chinese Medicine (CN), Jiangyin People's Hospital (CN)
Openalex Percentile: Top 16%
Osteoarthritis Treatment and Mechanisms
1.67
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