Published online Nov 26, 2020. doi: 10.4252/wjsc.v12.i11.1255
Peer-review started: June 28, 2020
First decision: August 9, 2020
Revised: August 19, 2020
Accepted: September 10, 2020
Article in press: September 10, 2020
Published online: November 26, 2020
Processing time: 151 Days and 3 Hours
There is accumulating evidence of an increased incidence of tendon disorders in people with diabetes mellitus. Diabetic tendinopathy is an important cause of chronic pain, restricted activity, and even tendon rupture in individuals. Tenocytes and tendon stem/progenitor cells (TSPCs) are the dominant cellular components associated with tendon homeostasis, maintenance, remodeling, and repair. Some previous studies have shown alterations in tenocytes and TSPCs in high glucose or diabetic conditions that might cause structural and functional variations in diabetic tendons and even accelerate the development and progression of diabetic tendinopathy. In this review, the biomechanical properties and histopathological changes in diabetic tendons are described. Then, the cellular and molecular alterations in both tenocytes and TSPCs are summarized, and the underlying mechanisms involved are also analyzed. A better understanding of the underlying cellular and molecular pathogenesis of diabetic tendinopathy would provide new insight for the exploration and development of effective therapeutics.
Core Tip: Tendinopathy is an important cause of chronic pain, restricted activity, and even tendon rupture in individuals with diabetes. Both tenocytes and tendon stem/progenitor cells (TSPCs) play essential roles in tendon maintenance, regeneration, and repair. In this review, we describe the biomechanical properties and histopathological changes in diabetic tendons. Then, we summarize the cellular and molecular alterations and the underlying mechanisms involved in tenocytes and TSPCs that might be associated with the development and progression of diabetic tendinopathy, providing clues for potential effective therapeutics for diabetic tendinopathy.