Faulty Lipid Transport Linked to Cell Senescence

UB study finds impaired ceramide transfer protein causes lipid buildup, triggering cellular limbo

Mar. 31, 2026 at 2:05am

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A highly textured, geometric abstract painting in earthy tones of green, brown, and ochre, depicting sweeping arcs, concentric circles, and precise botanical spirals to represent the complex cellular processes of lipid transport and accumulation that can trigger cellular senescence.An abstract visualization of the disrupted lipid transport that can lead to cellular senescence, a key factor in aging and age-related diseases.Buffalo Today

Researchers at the University at Buffalo have discovered that an impaired transport protein and a buildup of lipids known as ceramides can help lock cells into a state of replicative senescence, where they stop dividing permanently. The study found that during senescence, the ceramide transfer protein becomes disrupted, causing ceramides to accumulate inside the endoplasmic reticulum and trigger a stress response that pushes the cell to stop proliferating.

Why it matters

Replicative senescence protects against cancer by halting damaged cells, but as senescent cells accumulate, they may contribute to tissue decline and aging-related disease. Understanding the mechanisms behind this cellular limbo could offer insights into reversing some age-associated cellular abnormalities.

The details

The researchers found that ceramides, a group of fat molecules produced in the endoplasmic reticulum (ER), are normally transported by the ceramide transfer protein to the Golgi complex, where they are converted into another class of lipids. However, during replicative senescence, this transport process becomes impaired, causing ceramides to accumulate inside the ER and trigger a stress response that ultimately pushes the cell to stop dividing.

  • The study was published on March 30, 2026 in the journal Cell Chemical Biology.

The players

G. Ekin Atilla-Gokcumen

The study's corresponding author, Dr. Marjorie E. Winkler Distinguished Professor and associate chair in the UB Department of Chemistry.

Shweta Chitkara

The study's first author, a medicinal chemistry PhD student in Atilla-Gokcumen's lab.

Paras Prasad

SUNY Distinguished Professor in the UB departments of chemistry, physics, medicine and electrical engineering, and a co-author of the study.

Artem Pliss

A former UB research associate professor and now assistant professor at the D'Youville University School of Pharmacy, and a co-author of the study.

Mengru Li and Yasemin Sancak

Researchers at the University of Washington and co-authors of the study.

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What they’re saying

“It's as if a delivery route inside the cell becomes blocked, preventing ceramides from reaching their proper destination. When these lipid molecules can't be transported to the Golgi for processing, they begin to accumulate where they were made, inside the endoplasmic reticulum. That buildup appears to trigger stress signals that can ultimately push the cell to stop dividing.”

— G. Ekin Atilla-Gokcumen, Corresponding author, Dr. Marjorie E. Winkler Distinguished Professor and associate chair in the UB Department of Chemistry

“Ceramides are well known for accumulating at the mitochondria during apoptosis, where they help drive cell death. So when we saw ceramides building up in senescent cells, cells that are alive but no longer dividing, we had to ask: If they're not killing the cell, what are they doing?”

— Shweta Chitkara, First author, medicinal chemistry PhD student in Atilla-Gokcumen's lab

What’s next

The researchers plan to investigate whether correcting the disrupted ceramide transport pathway can restore healthier cellular function and potentially reverse some age-associated cellular abnormalities.

The takeaway

This study provides important insights into the role of lipid metabolism in cellular senescence, a process that contributes to aging and age-related diseases. Understanding the mechanisms behind this cellular limbo could lead to new strategies for maintaining cellular health and delaying the onset of age-related dysfunction.