Experimental and Molecular Medicine (Nov 2018)

Melatonin protects endothelial progenitor cells against AGE-induced apoptosis via autophagy flux stimulation and promotes wound healing in diabetic mice

  • Haiming Jin,
  • Zengjie Zhang,
  • Chengui Wang,
  • Qian Tang,
  • Jianle Wang,
  • Xueqin Bai,
  • Qingqing Wang,
  • Majid Nisar,
  • Naifeng Tian,
  • Quan Wang,
  • Cong Mao,
  • Xiaolei Zhang,
  • Xiangyang Wang

DOI
https://doi.org/10.1038/s12276-018-0177-z
Journal volume & issue
Vol. 50, no. 11
pp. 1 – 15

Abstract

Read online

Diabetes: Healing old wounds Melatonin, a sleep-regulating hormone, may speed wound healing in patients with diabetes by protecting blood-borne wound-healing cells known as endothelial progenitor cells (EPCs). In diabetes, EPCs become damaged, lose their capacity to migrate to wounds and form new tissue, and die prematurely. Delayed healing can lead to ulcers, infection, and sometimes amputation. Melatonin has recently been reported to promote wound healing, but the mechanism remains unclear. Xiangyang Wang and Xiaolei Zhang at Wenzhou Medical University, China, and coworkers hypothesized that melatonin might protect EPCs from diabetes-induced damage. They found that melatonin improved EPCs’ ability to eliminate damaged components, allowing them to repair themselves and restoring their wound-healing function. In further experiments, diabetic mice treated with melatonin healed faster than untreated mice. These results may help improve treatments for complications of diabetes.