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Replicative Cell Senescence

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Replicative cell senescence is a property of cells that allows them to divide a finite number of times throughout the organism's lifespan while preventing excessive proliferation. Replicative senescence is associated with the gradual loss of the telomere — short, repetitive DNA sequences found at the end of the chromosomes. Telomeres are bound by a group of proteins to form a protective cap on the ends of chromosomes. Embryonic stem cells express telomerase — an enzyme that adds...

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Updated: Apr 2, 2026

Techniques to Induce and Quantify Cellular Senescence

Techniques to Induce and Quantify Cellular Senescence

Published on: May 1, 2017

ER-localized ceramide accumulation contributes to replicative senescence.

Shweta Chitkara¹, Mengru Li², Natasha Gozali¹

¹Department of Chemistry, University at Buffalo, The State University of New York, Buffalo, NY 14260, USA.

Cell Chemical Biology

|March 31, 2026

Summary

This summary is machine-generated.

Altered ceramide trafficking disrupts cellular processes, leading to endoplasmic reticulum stress and promoting senescence. This study reveals ER-localized ceramide accumulation as a key factor in aging cells.

Keywords:

ER stress Raman BCA ceramide lipidomics organelle enrichment senescence transcriptomics

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Area of Science:

Cell Biology
Biochemistry
Molecular Biology

Background:

Ceramides are vital lipids regulating cellular functions through compartmentalized accumulation.
Mitochondrial ceramide accumulation is linked to apoptosis, but its role in senescence is unclear.
Understanding sphingolipid metabolism in cellular senescence is crucial for aging research.

Purpose of the Study:

To investigate the role of sphingolipid remodeling in replicative senescence.
To elucidate the mechanisms of ceramide accumulation and trafficking during senescence.
To determine the contribution of ceramide to endoplasmic reticulum stress in senescent cells.

Main Methods:

Lipidomics and transcriptomics were employed to analyze sphingolipid profiles.
Raman spectroscopy was used to assess ceramide localization within cells.
Biochemical assays and pharmacological inhibition of ceramide transfer protein (CERT) were performed.

Main Results:

Senescent cells showed elevated ceramide levels and reduced very-long-chain sphingomyelins.
Impaired ceramide-sphingomyelin turnover was indicated by unaltered sphingomyelin synthase 1 expression.
Inhibition of CERT mimicked sphingolipid changes and exacerbated senescence, with ER-localized ceramide accumulation confirmed.

Conclusions:

Disrupted ceramide trafficking contributes to ER stress and promotes cellular senescence.
ER-localized ceramide accumulation is a significant aspect of senescence-associated sphingolipid remodeling.
Targeting ceramide trafficking may offer therapeutic avenues for age-related diseases.