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Fig. 5 | Arthritis Research & Therapy

Fig. 5

From: Re-thinking osteoarthritis pathogenesis: what can we learn (and what do we need to unlearn) from mouse models about the mechanisms involved in disease development

Fig. 5

Comparison of TGF signalling in the cartilage, synovium, and bone in animal models of OA compared to human disease. Observations regarding TGF signalling activity in human disease have been limited to late-stage disease. Findings from animal models may aid in predicting the changes in TGF signalling that occur during early-stage disease in humans (grey text). One key point of difference in TGF signalling in mouse models compared to humans is that in mice, TGF-β3 is the most abundant TGF-β isoform in cartilage and the major form of TGF-β released in OA whereas in humans it is TGF-β1 (highlighted in red text). TGF-β1 and TGF-β3 have been shown to have different effects in other tissues. Whether they also have different effects on joint tissues in OA remains to be determined. The figure was created using Biorender.com

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Arthritis Research & Therapy

ISSN: 1478-6362

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