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SIRT3 ameliorates osteoarthritis via regulating chondrocyte autophagy and apoptosis through the PI3K/Akt/mTOR pathway

Kai Xu1, Yuzhe He1, Safwat Adel Abdo Moqbel1

  • 1Department of Orthopedics Surgery, The 2nd Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China.

International Journal of Biological Macromolecules
|February 8, 2021
PubMed

Insights

Sirtuin 3 (SIRT3) protects against osteoarthritis (OA) by reducing inflammation and cell damage. Overexpressing SIRT3 in rats alleviated joint damage, highlighting its therapeutic potential for this common joint disease.

Area of Science:

  • Biochemistry
  • Cell Biology
  • Pathology

Background:

  • Osteoarthritis (OA) is a prevalent degenerative joint disease.
  • Understanding molecular mechanisms underlying OA is crucial for developing effective treatments.

Purpose of the Study:

  • To investigate the role of Sirtuin 3 (SIRT3) in osteoarthritis (OA) pathophysiology.
  • To elucidate the underlying molecular mechanisms of SIRT3's function in OA.

Main Methods:

  • Utilized rat chondrocytes and a destabilized medial meniscus (DMM) rat model for in vitro and in vivo studies.
  • Employed lentivirus and plasmid for SIRT3 overexpression and siRNA for SIRT3 knockdown.
  • Administered intra-articular SIRT3 overexpression in a rat OA model.

Main Results:

  • SIRT3 overexpression inhibited IL-1β-induced inflammation, apoptosis, mitochondrial dysfunction, and chondrocyte degeneration.
  • SIRT3 overexpression restored IL-1β-induced autophagy inhibition and suppressed PI3K/Akt/mTOR signaling.
  • Intra-articular SIRT3 overexpression reduced the severity of OA-induced joint damage in rats.

Conclusions:

  • SIRT3 acts as a protective factor against osteoarthritis.
  • SIRT3 exerts its protective effects by inhibiting the PI3K/Akt/mTOR signaling pathway.
Keywords:
ApoptosisAutophagyOsteoarthritisPI3K/Akt/mTOR signalingSIRT3

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