Table 3.
Animal models of T2DM tendon injury and repair
Model | Injury type | Tendon | Outcomes compared to non-diabetic controls | Ref |
---|---|---|---|---|
C57BL6/J mouse DIO | Punch injury | FDL | ECM disorganization | 58 |
Limited tenocyte migration into granulation tissue | ||||
Decreased mechanical properties (max force, work to max force, stiffness) | ||||
C57BL6/J mouse DIO | Transection and repair | FDL | Increased gene expression of Col1, Col3, Mmp2, Mmp9 | 54 |
Increased protein expression of IL-1RA, TNFα, F4/80 | ||||
Altered macrophage polarization (increased/prolonged M2 activity) | ||||
Decreased mechanical properties (max force, work to max force, max load) | ||||
Decreased functional properties (decreased range of motion, increased gliding resistance) | ||||
Goto-Kakizaki rats | Transection | Achilles | ECM disorganization | 84 |
Decreased gene expression of Col1, Col3, Mmp-3 | ||||
Decreased stiffness | ||||
Decreased callus area | ||||
Goto-Kakizaki rats | Transection | Achilles | Decreased gene/protein expression of Tβ–4 and Vegf | 85 |
IL-1RA= interleukin-1 receptor antagonist, TNFα= tumor necrosis factor alpha, Tβ–4= thymosin beta-4, Vegf= vascular endothelial growth factor