Longevity PapersAbout
← All papers
RESEARCH PAPER / 2024-09-21

Metabolomics Dysfunction in Replicative Senescence of Periodontal Ligament Stem Cells Regulated by AMPK Signaling Pathway.

Meilin Hu, Ruiqi Liu, Xiaoyu Chen, Shen Yan, Jian Gao, Yao Zhang, Di Wu, Lu Sun, Zhi Jia, Guangyunhao Sun, Dayong Liu

Tianjin Key Laboratory of Oral Soft and Hard Tissues Restoration and Regeneration, Tianjin Medical University School of Stomatology, Tianjin Medical University, Heping, China. · pubmed

Abstract

Periodontal ligament mesenchymal stem cells (PDLSCs) are a promising cell resource for stem cell-based regenerative medicine in dentistry, but they inevitably acquire a senescent phenotype after prolonged in vitro expansion. The key regulators of PDLSCs during replicative senescence remain unclear. Here, we sought to elucidate the role of metabolomic changes in determining the cellular senescence of PDLSCs. PDLSCs were cultured to passages 4, 10, and 20. The senescent phenotypes of PDLSCs were detected, and metabolomics analysis was performed. We found that PDLSCs manifested senescence phenotype during passaging. Metabolomics analysis showed that the metabolism of replicative senescence in PDLSCs varied significantly. The AMP-activated protein kinase (AMPK) signaling pathway was closely related to adenosine monophosphate (AMP) levels. The AMP:ATP ratio increased in senescent PDLSCs; however, the levels of p-AMPK,

The following analysis is generated by AI and may contain errors. It is separate from the authors’ abstract and is not peer review.

Research summary

The paper investigates the metabolomic changes associated with replicative senescence in periodontal ligament stem cells, which is relevant to understanding cellular aging processes. However, while it contributes to the knowledge of stem cell behavior and the role of AMPK signaling in senescence, the findings are more incremental than groundbreaking. The implications for longevity research are limited, as the focus is on a specific cell type in a dental context rather than broader mechanisms of aging or lifespan extension.

Author of this paper? Send a correction.