학술논문

The role of melatonin in bone regeneration: A review of involved signaling pathways.
Document Type
Article
Source
Biochimie. Nov2022, Vol. 202, p56-70. 15p.
Subject
*BONE regeneration
*CELLULAR signal transduction
*VITAMIN K2
*BONE density
*BONE resorption
*MELATONIN
Language
ISSN
0300-9084
Abstract
Increasing bone resorption followed by decreasing bone mineralization are hallmarks of bone degeneration, which mostly occurs in the elderly population and post-menopausal women. The use of mesenchymal stem cells (MSCs) has raised many promises in the field of bone regeneration due to their high osteoblastic differentiation capacity and easy availability from abundant sources. A variety of compounds, including growth factors, cytokines, and other internal factors, have been combined with MSCs to increase their osteoblastic differentiation capacity. One of these factors is melatonin, whose possible regulatory role in bone metabolism and formation has recently been suggested by many studies. Melatonin also is a potential signaling molecule and can affect many of the signaling pathways involved in MSCs osteoblastic differentiation, such as activation of PI3K/AKT, BMP/Smad, MAPK, NFkB, Nrf2/HO-1, Wnt, SIRT/SOD, PERK/ATF4. Furthermore, melatonin in combination with other components such as strontium, vitamin D3, and vitamin K2 has a synergistic effect on bone microstructure and improves bone mineral density (BMD). In this review article, we aim to summarize the regulatory mechanisms of melatonin in osteoblastic differentiation of MSCs and underling involved signaling pathways as well as the clinical potential of using melatonin in bone degenerative disorders. • Melatonin can increase MSC's osteoblastic differentiation. • Stimulating of MSCs osteoblastic differentiation is an important strategy to cure bone degenerative diseases such as osteoporosis. • Many cellular signaling pathways are involved in the melatonin effect in MSCs osteoblastic differentiation. • The combination of melatonin with vitamins involved in bone formation and osteoporosis drugs can improve bone regeneration in patients with bone degenerative diseases. [ABSTRACT FROM AUTHOR]