《生命科学》 2023, 35(10): 1366-1371

糖尿病腱病研究进展

连红强 , 张丽蓉 , 赵常红^*

西北师范大学体育学院，兰州 730030

摘　要：

糖尿病腱病患病率较高，糖尿病引起肌腱组织结构改变，肌腱刚度、最大负载、杨氏模量下降。肌腱细胞及肌腱干细胞在高血糖和晚期糖基化终末产物作用下功能受损。糖尿病引起肌腱神经损伤、胶原蛋白合成减少、炎症因子异常释放、胰岛素样生长因子产生减少，损伤肌腱组织愈合延迟导致肌腱退变。损伤肌腱新生血管增加，基质形成和成纤维细胞增殖依赖于血管生成。糖尿病腱病发病机制较为复杂，本文通过综述糖尿病腱病发病相关分子机制，凝练糖尿病腱病相关信号通路，旨在为糖尿病腱病研究提供理论依据。

通讯作者：赵常红 , Email:changhongzhao@126.com

Research progress of diabetes tendon disease

LIAN Hong-Qiang , ZHANG Li-Rong , ZHAO Chang-Hong^*

College of Physical Education of Northwest Normal University, Lanzhou 730030, China

Abstract:

The prevalence of diabetic tendinopathy is high, and diabetes causes structural changes in tendon tissue, with decreases in tendon stiffness, maximum load, and Young's modulus. Tendon cells and tendon stem cells are functionally impaired by hyperglycemia and advanced glycosylation end products. Diabetes causes tendon nerve damage, decreased collagen synthesis, abnormal release of inflammatory factors, decreased insulin-like growth factor production, and delayed healing of injured tendon tissue leading to tendon degeneration. Neovascularization increases after tendon injury, and matrix formation and fibroblast proliferation are dependent on angiogenesis. The pathogenesis of diabetic tendinopathy is complex, this paper reviews the molecular mechanisms related to the pathogenesis of diabetic tendinopathy and condenses the signaling pathways related to diabetic tendinopathy, aiming to provide a theoretical basis for the study of diabetic tendinopathy.

Communication Author：ZHAO Chang-Hong , Email:changhongzhao@126.com