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FGF1 reduces cartilage injury in osteoarthritis via regulating AMPK/Nrf2 pathway

Yun-Xuan Li1, Jun Shu1, Nan-Nan Kou1

  • 1Department of Traumatology, The Second Affiliated Hospital of Kunming Medical University, 374 Dianmian Avenue, Wuhua District, Kunming, 650000, Yunnan, China.

Journal of Molecular Histology
|September 2, 2023
PubMed

Insights

Fibroblast growth factor 1 (FGF1) knockdown shows protective effects against osteoarthritis (OA) by activating AMPK and Nrf2 pathways. This study reveals FGF1

Area of Science:

  • Biochemistry
  • Molecular Biology
  • Orthopedics

Background:

  • Osteoarthritis (OA) is a degenerative joint disease influenced by cytokines and growth factors.
  • Fibroblast growth factor 1 (FGF1) role in OA pathogenesis requires further elucidation.
  • Oxidative stress and specific molecular pathways are implicated in OA cartilage destruction.

Purpose of the Study:

  • To investigate the protective effects of fibroblast growth factor 1 (FGF1) knockdown on osteoarthritis.
  • To elucidate the underlying molecular mechanisms of FGF1's involvement in OA.
  • To evaluate the in vivo efficacy of FGF1 modulation in OA models.

Main Methods:

  • In vitro studies involving FGF1 knockdown in chondrocytes.
  • In vivo evaluation using destabilization of the medial meniscus (DMM) and anterior/posterior cruciate ligament transection models.
  • Analysis of protein expression (Nrf2, HO-1) and phosphorylation (AMPK).
  • Knockdown experiments targeting Nrf2 and AMPK to assess their roles.

Main Results:

  • FGF1 knockdown reversed oxidative damage in osteoarthritis models.
  • FGF1 knockdown increased protein expression of Nrf2 and HO-1, linked to AMPK phosphorylation.
  • Nrf2 knockdown abolished the antioxidant effects of FGF1 knockdown on chondrocytes.
  • AMPK knockdown negated the protective impact of FGF1 knockdown in OA.

Conclusions:

  • FGF1 knockdown demonstrates a significant protective effect against osteoarthritis.
  • The mechanism involves the activation of AMPK and Nrf2 pathways in articular chondrocytes.
  • Targeting FGF1 offers a potential therapeutic strategy for preventing and reversing OA.
Keywords:
Amp-activated protein kinaseFibroblast growth factor 1Nuclear factor erythroid 2 related factor 2Osteoarthritis

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