Human Amniotic Mesenchymal Stem Cells Promote Endogenous Bone Regeneration

Bone regeneration has become a research hotspot and therapeutic target in the field of bone and joint medicine. Stem cell-based therapy aims to promote endogenous regeneration and improves therapeutic effects and side-effects of traditional reconstruction of significant bone defects and disorders. H...

Full description

Saved in:
Bibliographic Details
Published in:Frontiers in endocrinology (Lausanne) 2020-10, Vol.11, p.543623-543623
Main Authors: Li, Jin, Zhou, Zhixuan, Wen, Jin, Jiang, Fei, Xia, Yang
Format: Article
Language:English
Subjects:
Amnion - cytology
Animals
arthritis
bone defects
Bone Regeneration
clinical trials
Endocrinology
endogenous bone regeneration
hAMSCs
Humans
Joint Diseases - therapy
Mesenchymal Stem Cell Transplantation - methods
Mesenchymal Stem Cells - physiology
Osteogenesis
paracrine functions
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Bone regeneration has become a research hotspot and therapeutic target in the field of bone and joint medicine. Stem cell-based therapy aims to promote endogenous regeneration and improves therapeutic effects and side-effects of traditional reconstruction of significant bone defects and disorders. Human amniotic mesenchymal stem cells (hAMSCs) are seed cells with superior paracrine functions on immune-regulation, anti-inflammation, and vascularized tissue regeneration. The present review summarized the source and characteristics of hAMSCs and analyzed their roles in tissue regeneration. Next, the therapeutic effects and mechanisms of hAMSCs in promoting bone regeneration of joint diseases and bone defects. Finally, the clinical application of hAMSCs from current clinical trials was analyzed. Although more studies are needed to confirm that hAMSC-based therapy to treat bone diseases, the clinical application prospect of the approach is worth investigating.
ISSN:1664-2392
1664-2392
DOI:10.3389/fendo.2020.543623