The age pigment lipofuscin causes oxidative stress, lysosomal dysfunction, and pyroptotic cell death.

Tim Baldensperger, Tobias Jung, Tom Heinze, Tanja Schwerdtle, Annika Höhn, Tilman Grune

Department of Molecular Toxicology, German Institute of Human Nutrition Potsdam-Rehbruecke (DIfE), Arthur-Scheunert-Allee 114-116, 14558 Nuthetal, Germany; Institute of Biological Chemistry, Faculty of Chemistry, University of Vienna, Währinger Straße 38, 1090 Vienna, Austria. Electronic address: [email protected] of Molecular Toxicology, German Institute of Human Nutrition Potsdam-Rehbruecke (DIfE), Arthur-Scheunert-Allee 114-116, 14558 Nuthetal, Germany; Institute of Biological Chemistry, Faculty of Chemistry, University of Vienna, Währinger Straße 38, 1090 Vienna, Austria. Electronic address: [email protected]. · pubmed

Paper

Abstract

Accumulation of the age pigment lipofuscin represents a ubiquitous hallmark of the aging process. However, our knowledge about cellular effects of lipofuscin accumulation is potentially flawed, because previous research mainly utilized highly artificial methods of lipofuscin generation. In order to address this tremendous problem, we developed a convenient protocol for isolation of authentic lipofuscin from human and equine cardiac tissue in high purity and quantity. Isolated lipofuscin aggregates contained elevated concentrations of proline and metals such as calcium or iron. The material was readily incorporated by fibroblasts and caused cell death at low concentrations (LC

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Research summary

The paper addresses the accumulation of lipofuscin, which is linked to the aging process and cellular dysfunction. It presents a method for isolating authentic lipofuscin, which could provide insights into its role in aging and age-related cellular damage. However, while it contributes to understanding a hallmark of aging, the findings appear to be incremental rather than groundbreaking, limiting its overall impact on the field of longevity research.

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