FTO Suppresses Dental Pulp Stem Cell Senescence By Destabilizing Nolc1 Mrna

Aging Pathway
Therapeutic
The protein FTO prevents the aging of dental pulp stem cells by destabilizing NOLC1 messenger RNA, which otherwise promotes cellular aging.
Author

Gemini

Published

December 4, 2025

Our bodies contain special cells called stem cells, which have the remarkable ability to repair and regenerate tissues. Dental pulp stem cells, found within our teeth, are particularly important for dental health and potential regenerative therapies. However, like all cells, they undergo a process called senescence, or cellular aging, which limits their ability to function and repair.

Recent research has shed light on a key player in this aging process: a protein known as FTO. Scientists observed that as dental pulp stem cells age, the amount of FTO protein decreases. When FTO levels are low, these stem cells age more quickly and lose their regenerative capacity. Conversely, increasing the amount of FTO can help these cells stay “younger” for longer.

The study uncovered the mechanism behind FTO’s protective role. FTO works by targeting a specific messenger RNA (mRNA) molecule called NOLC1. Messenger RNA acts as a blueprint for making proteins, and its stability dictates how much protein is produced. FTO destabilizes NOLC1 mRNA, meaning it helps break it down, leading to lower levels of the NOLC1 protein.

Why is this important? Because high levels of NOLC1 protein were found to actively promote the aging of dental pulp stem cells. Essentially, FTO acts as a brake on NOLC1, preventing it from accelerating cellular aging. This regulation involves a chemical tag on the NOLC1 mRNA called m6A, which FTO removes. Without FTO, this tag makes NOLC1 mRNA more stable, resulting in more NOLC1 protein and faster aging.

This discovery highlights a crucial pathway involving FTO, NOLC1, and another well-known aging-related protein called p53. Understanding this pathway provides new insights into how dental pulp stem cells age and offers potential strategies to prevent their decline, which could significantly benefit regenerative dentistry and stem cell-based treatments.


Source: link to paper