FIGURE 2  Major structural and molecular changes in chronic tendinopathy.

From the following article:

Tendinopathy—from basic science to treatment

Graham Riley

Nature Clinical Practice Rheumatology (2008) 4, 82-89
doi:10.1038/ncprheum0700

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Figure 2.  Major structural and molecular changes in chronic tendinopathy.

Typical features of tendinopathy are cell rounding and increased cell number, proteoglycan content and vascularity. Major molecular changes that have been identified by gene-expression studies, protein analysis or both are summarized. Molecules for which expression levels are increased are denoted by an upwards arrow, molecules for which expression levels are decreased are denoted by a downwards arrow and molecules for which expression levels remain unchanged are denoted by a horizontal arrow. Note that not all the changes shown have been rigorously confirmed, particularly at the protein level. Photomicrograph (A) is an alcian blue/H&E-stained section of supraspinatus tendinopathy, showing proteoglycans stained blue. Photomicrograph (B) is an H&E-stained section of Achilles tendinopathy, showing increased cellularity and proliferation of blood vessels. Abbreviations: ADAM, a disintegrin and metalloproteinase; ADAMTS, ADAM with thrombospondin motifs; AGE, advanced glycation end product; COX2, cyclo-oxygenase 2; H&E, hemotoxylin and eosin; IGF-I, insulin-like growth factor 1; MMP, matrix metalloproteinase; NMDAR, N-methyl-D-aspartate receptor; PDGFR, platelet-derived growth factor receptor; PGE2, prostaglandin E2; TGF-beta, transforming growth factor beta; TGF-betaR1, TGF-beta type 1 receptor; VEGF, vascular endothelial growth factor.

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