Lipofuscin

Formation, Distribution, and Metabolic Consequences

Authors


Address for correspondence: Tilman Grune, Institute for Biological Chemistry and Nutrition, University of Hohenheim, Garbestrasse 28, 70593 Stuttgart, Germany 70593. Voice: +49-711-459-24060; fax: +49-711-459-23386.
 grune@uni-hohenheim.de

Abstract

Abstract: One of the highlights of postmitotic aging is the intracellular accumulation of highly oxidized and cross-linked proteins, known as lipofuscin. Lipofuscin is insoluble and not degradable by lysosomal enzymes or the proteasomal system, which is responsible for the recognition and degradation of misfolded and oxidatively damaged proteins. These aggregates have been found in various cell types, including heart, liver, kidney, neuronal tissue, and dermal tissue, and are associated with the life span of a single postmitotic cell and, consequently, of the whole organism. Lipofuscin formation appears to depend on the rate of oxidative damage to proteins, the functionality of mitochondrial repair systems, the proteasomal system, and the functionality and effectiveness of the lysosomes. This review highlights the current knowledge of the formation, distribution, and effects of lipofuscin in mammalian cells.

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