Published on: Feb 02, 2026
Advances in public health have extended human lifespan, but many people spend these added years affected by chronic diseases such as cancer, diabetes, and Alzheimer’s disease. Aging itself is the strongest risk factor for most of these conditions, raising a critical question: can we uncouple aging from disease to extend healthspan, not just lifespan?
The laboratory of Kris Burkewitz, assistant professor of cell and developmental biology, seeks to answer this by studying how cells organize their internal structures, or organelles, and how these architectures influence metabolism, function, and disease risk. In a recent study published in Nature Cell Biology, the Burkewitz lab identified a previously underexplored aging mechanism active remodeling of the endoplasmic reticulum (ER) through a selective process known as ER-phagy.
Using advanced genetic tools and high-resolution microscopy in Caenorhabditis elegans, the team showed that aging cells selectively reduce rough ER, which is involved in protein production, while largely preserving tubular ER linked to lipid metabolism. This structural reorganization aligns with known features of aging, including impaired protein maintenance and metabolic shifts.
Importantly, ER-phagy was found to be directly linked to lifespan and healthy aging, positioning it as a promising therapeutic target for age-related neurodegenerative and metabolic diseases. Because ER remodeling occurs early in the aging process, it may act as a trigger for later cellular dysfunction offering a potential window for intervention to preserve cellular health over time.
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