As a connective tissue, tendon connects the muscle and bone, and plays the key role in the locomotor system. Some previous studies have shown the pathological alternations in diabetic tendons, which might result in the structural and functional changes, and even accelerate the process of diabetic foot. In this review, we examined the current findings of the diabetic tendons in the form of various aspects, and summarized the clinical presentation, imaging, biomechanical, histopathological, cellular and molecular abnormalities in the diabetic tendons. The progress of diabetic tendon damage is complicated and the main hypotheses include the excessive accumulation of AGEs, the altered inflammatory response, neovascularization and insensitive neuropathy. However, the cellular and molecular mechanisms of these alterations are still ambiguous. Tendon stem/progenitor cells (TSPCs) have been discovered to play important roles in both tendon physiology and tendon pathology. Recently, we identified TSPCs from patellar tendons in our well-established diabetic rat model and found impaired tenogenic differentiation potential of these cells. We proposed a new hypothesis that the impaired cell functions of diabetic TSPCs might be the underlying cellular and molecular mechanism of the diabetic tendon alternations. These findings should be helpful to establish a better therapeutic strategy for diabetic tendon repair and regeneration.