Published online Sep 26, 2021. doi: 10.4252/wjsc.v13.i9.1338
Peer-review started: April 6, 2021
First decision: May 12, 2021
Revised: May 26, 2021
Accepted: August 17, 2021
Article in press: August 17, 2021
Published online: September 26, 2021
Tendinopathy is a challenging complication observed in patients with diabetes mellitus. Tendinopathy usually leads to chronic pain, limited joint motion, and even ruptured tendons. Imaging and histological analyses have revealed pathological changes in various tendons of patients with diabetes, including disorganized arrangement of collagen fibers, microtears, calcium nodules, and advanced glycation end product (AGE) deposition. Tendon-derived stem/ progenitor cells (TSPCs) were found to maintain hemostasis and to participate in the reversal of tendinopathy. We also discovered the aberrant osteochondrogenesis of TSPCs in vitro. However, the relationship between AGEs and TSPCs in diabetic tendinopathy and the underlying mechanism remain unclear. In this review, we summarize the current findings in this field and hypothesize that AGEs could alter the properties of tendons in patients with diabetes by regulating the proliferation and differentiation of TSPCs in vivo.
Core Tip: Patients with diabetic tendinopathy usually suffer from chronic pain, restricted joint motion, calcium deposition, and even tendon rupture. Advanced glycation end products (AGEs) have been shown to affect tendon biology and biomechanical properties. In addition, tendon-derived stem/progenitor cells (TSPCs) play an important role in tendon hemostasis, regeneration, and repair. However, the relationships between diabetic tendinopathy, AGEs, and TSPCs remain unclear. Thus, in this review, we summarize the current findings and discuss the possible relationships between AGEs and TSPCs. This might provide new guidance for the development of effective treatments for diabetic tendinopathy.