中国神经再生研究(英文版) ›› 2023, Vol. 18 ›› Issue (4): 760-762.doi: 10.4103/1673-5374.353480

• 综述:神经损伤修复保护与再生 • 上一篇    下一篇

褪黑激素、隧道纳米管间充质细胞和组织再生

  

  • 出版日期:2023-04-15 发布日期:2022-10-27

Melatonin, tunneling nanotubes, mesenchymal cells, and tissue regeneration

Francesca Luchetti1, *, Silvia Carloni1, Maria G. Nasoni1, Russel J. Reiter2, Walter Balduini1, *   

  1. 1Department of Biomolecular Sciences, University of Urbino Carlo Bo, Urbino, Italy;  2Department of Cell Systems and Anatomy, Long School of Medicine, UT Health, San Antonio, TX, USA
  • Online:2023-04-15 Published:2022-10-27
  • Contact: Walter Balduini, PhD, walter.balduini@uniurb.it; Francesca Luchetti, PhD, francesca.luchetti@uniurb.it.
  • Supported by:
    This work was supported by the University of Urbino Carlo Bo (No. DR-473_2018) to WB. 

摘要: https://orcid.org/0000-0001-8438-9559 (Walter Balduini); https://orcid.org/0000-0002-8225-3129 (Francesca Luchetti)

Abstract: Mesenchymal stem cells are multipotent stem cells that reside in many human tissues and organs. Mesenchymal stem cells are widely used in experimental and clinical regenerative medicine due to their capability to transdifferentiate into various lineages. However, when transplanted, they lose part of their multipotency and immunomodulatory properties, and most of them die after injection into the damaged tissue. In this review, we discuss the potential utility of melatonin in preserving mesenchymal stem cells’ survival and function after transplantation. Melatonin is a pleiotropic molecule regulating critical cell functions including apoptosis, endoplasmic reticulum stress, and autophagy. Melatonin is also synthesized in the mitochondria where it reduces oxidative stress, the opening of the mitochondrial permeability transition pore and the downstream caspase activation, activates uncoupling proteins, and curtails the proinflammatory response. In addition, recent findings showed that melatonin also promotes the formation of tunneling nanotubes and the transfer of mitochondria between cells through the connecting tubules. As mitochondrial dysfunction is a primary cause of mesenchymal stem cells death and senescence and a critical issue for survival after transplantation, we propose that melatonin by favoring mitochondria functionality and their transfer through tunneling nanotubes from healthy to suffering cells could improve mesenchymal stem cell-based therapy in a large number of diseases for which basic and clinical trials are underway. 

Key words: brain ischemia, cell transplantation, melatonin, mesenchymal stem cell, mitochondria, mitochondrial transplantation, regenerative therapy, senescence, tunneling nanotubes