Figure - PMC

Skip to main content

An official website of the United States government

Here's how you know

Here's how you know

Official websites use .gov
A .gov website belongs to an official government organization in the United States.

Secure .gov websites use HTTPS
A lock ( ) or https:// means you've safely connected to the .gov website. Share sensitive information only on official, secure websites.

View full-text article in PMC

. 2023 Dec 26;15(12):1093–1103. doi: 10.4252/wjsc.v15.i12.1093

Search in PMC
Search in PubMed
View in NLM Catalog
Add to search

©The Author(s) 2023. Published by Baishideng Publishing Group Inc. All rights reserved.

This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial.

PMC Copyright notice

Graphical summary of the study findings. High glucose impaired the mitochondrial function in mesenchymal stem cells (MSCs) by perturbing many mitochondrial regulatory dynamics and factors, particularly mitochondrial membrane potential, nicotinamide adenine dinucleotide (NAD+)/NADH pool, and mammalian target of rapamycin protein. This mitochondrial dysfunction is associated with triggering apoptosis in MSCs, which mechanistically explained the poor survival of MSCs in hyperglycemia. MSCs: Mesenchymal stem cells; PI3K: Phosphatidylinositol 3-kinase; mTOR: Mammalian target of rapamycin; NAD+: Nicotinamide adenine dinucleotide.