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Peer-reviewedCC BY 4.0PLOS One

Isoquercitrin ameliorates chondrocyte dysfunction in osteoarthritis by targeting AKT1-mediated mitochondrial dynamics regulation

  • Yuan Ding1
  • Xiang Wang2
  • Shihua Zong
  • Qiong Wen
  • Luyang Zhang
  1. 1Department of Rheumatology and Immunology, Yantaishan Hospital, Yantai, Shandong Province, China
  2. 2Department of Nephrology, Yantaishan Hospital, Yantai, Shandong Province, China
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Abstract

Osteoarthritis (OA), a prevalent degenerative joint disorder, is driven by chondrocyte anabolic-catabolic imbalance, aberrant inflammation, and mitochondrial dysfunction. 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 AKT1. 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 AKT1 overexpression abolishes its protective effects—confirming AKT1 as a key mediator. 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 AKT1 targeting to chondroprotection.

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Cite

BibTeXRIS
BibTeX
@article{ding2026isoquercitrin,
  title = {{Isoquercitrin ameliorates chondrocyte dysfunction in osteoarthritis by targeting AKT1-mediated mitochondrial dynamics regulation}},
  author = {Yuan Ding and Xiang Wang and Shihua Zong and Qiong Wen and Luyang Zhang},
  journal = {PLOS One},
  year = {2026},
  month = sep,
  doi = {10.1371/journal.pone.0357989},
  url = {https://doi.org/10.1371/journal.pone.0357989},
  note = {CC BY 4.0},
}
RIS
TY  - JOUR
TI  - Isoquercitrin ameliorates chondrocyte dysfunction in osteoarthritis by targeting AKT1-mediated mitochondrial dynamics regulation
AU  - Yuan Ding
AU  - Xiang Wang
AU  - Shihua Zong
AU  - Qiong Wen
AU  - Luyang Zhang
PY  - 2026
DA  - 2026/09/17
JO  - PLOS One
DO  - 10.1371/journal.pone.0357989
UR  - https://doi.org/10.1371/journal.pone.0357989
AB  - Osteoarthritis (OA), a prevalent degenerative joint disorder, is driven by chondrocyte anabolic-catabolic imbalance, aberrant inflammation, and mitochondrial dysfunction. 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 AKT1. 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 AKT1 overexpression abolishes its protective effects—confirming AKT1 as a key mediator. 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 AKT1 targeting to chondroprotection.
SN  - 1932-6203
ER  -