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Table · dataset · 2026

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<div><p>Osteoarthritis (OA), a prevalent degenerative joint disorder, is driven by chondrocyte anabolic-catabolic imbalance, aberrant inflammation, and mitochondrial dysfunction.

Description

Disease-modifying therapies targeting these pathological processes remain scarce, limiting effective clinical intervention. Herein, we demonstrate an isoquercitrin (IQ)-based chondroprotective strategy that rectifies osteoarthritis-related chondrocyte impairment by targeting <i>AKT1</i>.

IQ first reverses IL-1β-induced chondrocyte proliferation arrest, shifts metabolic homeostasis toward anabolism, and mitigates pro-inflammatory responses. It simultaneously restores mitochondrial homeostasis by normalizing dynamic balance. Mechanistically, IQ binds to AKT1 with high affinity, and <i>AKT1</i> overexpression abolishes its protective effects—confirming <i>AKT1</i> as a key mediator.

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This approach re-establishes chondrocyte functional homeostasis by coupling anti-inflammatory, metabolic-regulatory, and mitochondrial-stabilizing activities. This work highlights IQ as a promising candidate for osteoarthritis intervention and provides a mechanistic framework linking <i>AKT1</i> targeting to chondroprotection.</p></div>

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Provenance · 1 source records, 20 field assertions
SourceKeyLast seenRaw
figshareoai:figshare.com:article/3390354010 d agoJSON v1
FieldAssertionExtractorEvidence
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