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Updated: May 15, 2026

Techniques to Induce and Quantify Cellular Senescence

Techniques to Induce and Quantify Cellular Senescence

Published on: May 1, 2017

Senescence regulation by mTOR.

Vjekoslav Dulic¹

¹Institut de Génétique Moléculaire, Montpellier, France. vjekoslav.dulic@igmm.cnrs.fr

Methods in Molecular Biology (Clifton, N.J.)

|January 9, 2013

Summary

This summary is machine-generated.

Cellular senescence, a key aging process, is linked to the mTOR pathway, a regulator of cell growth. This review explores their connection, highlighting the tumor suppressor p53

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Induction and Validation of Cellular Senescence in Primary Human Cells

Induction and Validation of Cellular Senescence in Primary Human Cells

Published on: June 20, 2018

Area of Science:

Cellular biology
Molecular biology
Gerontology

Background:

Cellular senescence is an irreversible cell cycle arrest triggered by stress.
The mTOR pathway regulates cell metabolism and growth.
The tumor suppressor p53 is a common regulator of both senescence and mTOR signaling.

Purpose of the Study:

To review the evidence linking cellular senescence and the mTOR pathway.
To highlight the role of p53 in connecting these two processes.
To discuss the controversial role of mTOR in senescence and its implications for aging.

Main Methods:

Literature review of recent research on senescence, mTOR, and p53.
Analysis of studies investigating the interplay between these pathways.
Synthesis of current understanding and identification of research gaps.

Main Results:

Evidence suggests a link between cellular senescence and mTOR signaling.
The tumor suppressor p53 plays a critical role in integrating these pathways.
Recent findings offer new insights into the debated role of mTOR in senescence.

Conclusions:

The connection between senescence and mTOR, mediated by p53, is crucial for understanding aging.
Further research is needed to fully elucidate the complex role of mTOR in senescence.
This field holds significant relevance for aging research and age-related diseases.