An extensive review regarding the adipokines in the pathogenesis and progression of osteoarthritis.

Osteoarthritis is the most prevalent form of aging-related joint diseases, and its etiology is still not fully understood. Obesity has been recognized as one of the most significant and potentially preventable risk factors for osteoarthritis. Beyond mechanical loading, adipokines, including leptin, visfatin, adiponectin, resistin and others, are demonstrated to have metabolic implications in the pathogenesis and progression in obesity-induced osteoarthritis by modulating the pro/anti-inflammatory and anabolic/catabolic balance, apoptosis, matrix remodeling and subchondral bone ossification. Accordingly, adipokines emerge as potential candidates to link these two entities, and may serve as putative targets for disease-modifying drugs for osteoarthritis, especially for obese patients. Here we summarize studies over the past decades on the pivotal role of adipokine family in osteoarthritis, and aim to shed a light on the causative link between obesity and osteoarthritis. Notably, due to difficulties in separation of the metabolic effect from the mechanical effect of fat excess, researches on osteoarthritis in non-weight-bearing joints may provide a promising direction and more emphasis shall be put on them in future.

• Publication year

  2019

• Venue

  Cytokine

• Publication date

  Unknown publication date

• Fields of study

  Biology, Medicine

• Identifiers
  DOI 10.1016/j.cyto.2018.06.019PMID 30539776
• External record

  Open on Semantic Scholar

• Source metadata

  Semantic Scholar, PubMed

• No claims are published for this paper.

• No concepts are published for this paper.

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