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Role of the Inflammation-Autophagy-Senescence Integrative Network in Osteoarthritis

Claire Vinatier1,2, Eduardo Domínguez3, Jerome Guicheux1,2,4

  • 1INSERM, UMR 1229, Regenerative Medicine and Skeleton, University of Nantes, ONIRIS, Nantes, France.

Frontiers in Physiology
|July 11, 2018
PubMed

Insights

This review highlights preclinical models for osteoarthritis (OA) and cartilage aging, focusing on cellular senescence and inflammation. Findings suggest novel therapeutic targets for disease modification in OA.

Area of Science:

  • Gerontology
  • Rheumatology
  • Molecular Biology

Background:

  • Osteoarthritis (OA) is a leading cause of chronic disability, characterized by cartilage degeneration.
  • Understanding cartilage aging, chondrocyte senescence, inflammation, and autophagy is crucial for developing OA therapies.

Purpose of the Study:

  • To review recent mechanistic and therapeutic preclinical models of aging relevant to articular cartilage and OA.
  • To identify promising molecular targets and pathways for OA treatment.

Main Methods:

  • Literature review of preclinical models and molecular mechanisms in cartilage aging and OA.
  • Analysis of evidence linking metabolism, senescence, and circadian rhythms to joint degeneration.

Main Results:

  • Cellular senescence, inflammation, and autophagy are key mechanisms in OA pathogenesis.
  • Metabolism, nuclear receptors, transcription factors, and circadian rhythms play significant roles in musculoskeletal degeneration.

Conclusions:

  • Preclinical models offer insights into molecular mechanisms of joint degeneration.
  • Translational research focusing on identified pathways could lead to novel disease-modifying OA therapies.
Keywords:
OAagingautophagycartilagechondrocytesinflammationsenescencetherapeutics

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