Lipofuscin: mechanisms of age-related accumulation and influence on cell function.

  title={Lipofuscin: mechanisms of age-related accumulation and influence on cell function.},
  author={Ulf T. Brunk and Alexei Terman},
  journal={Free radical biology \& medicine},
  volume={33 5},

Dynamic Scaling of Lipofuscin Deposition in Aging Cells

A model of non-equilibrium cluster growth and aggregation that is developed for studying the formation and growth of lipofuscin is introduced and an unusual feature of this model is that while small particles are removed from the cell the larger ones become fixed and grow by aggregation.

Lipofuscin: formation, distribution, and metabolic consequences.

This review highlights the current knowledge of the formation, distribution, and effects of lipofuscin in mammalian cells and investigates the role of mitochondria repair systems and the functionality and effectiveness of the lysosomes.

Increased resistance of lipofuscin-loaded prematurely senescent fibroblasts to starvation-induced programmed cell death

Disturbed apoptotic response found in lipofuscin-loaded cells can be interpreted as an example of hormesis—an adaptation to low doses of otherwise harmful agents, in this case of lip ofuscin, which has a protective effect at moderate amounts but becomes toxic at large quantities.

Lipofuscin and aging: a matter of toxic waste.

Accumulating evidence suggests that lipofuscin is not benign but can impair the functioning of seemingly unrelated cellular systems, including the ubiquitin/proteasome pathway.

Occurrence and characterization of lipofuscin and ceroid in human atherosclerotic plaque

The present study investigates the occurrence and distribution of lipofuscin and ceroid in human atherosclerotic plaque and adjacent healthy tissues and analyzes the ultrastructural changes associated with their accumulation within the cell.

Can lipofuscin accumulation be prevented?

  • T. Kurz
  • Biology, Chemistry
    Rejuvenation research
  • 2008
It is suggested that pulse doses of iron chelators that easily penetrate membranes could be used to diminish lipofuscinogenesis.

Mitochondrial Autophagy and Lipofuscin Accumulation in Aging Odontoblasts

Age-related changes in odontoblasts are observed as a long-term process in which the progressive accumulation of intralysosomal debris limits the autophagic turnover of mitochondrial components, causing an eventual decline in physiological cell functions, which leads to increased vulnerability under stress conditions.

Lysosome-targeted stress reveals increased stability of lipofuscin-containing lysosomes

It is suggested that lipofuscin exerts lysosome-stabilizing properties and was less affected or even preserved in case of lip ofuscin-loaded cells.



Lipofuscin: Mechanisms of formation and increase with age

  • A. TermanU. Brunk
  • Biology
    APMIS : acta pathologica, microbiologica, et immunologica Scandinavica
  • 1998
The present knowledge of age pigment formation is outlined, possible mechanisms responsible for the increase of lipofuscin with age are considered, and oxidative reactions are considered to act as age‐independent enhancers of lip ofuscin accumulation.

Lipofuscin accumulation in cultured retinal pigment epithelial cells reduces their phagocytic capacity.

Severe lipofuscin accumulation of RPE cells appears to result in a greatly decreased phagocytic capacity, which may well be of significance in the development of age-related macular degeneration.

Inhibition of lysosomal degradative functions in RPE cells by a retinoid component of lipofuscin.

The findings indicate that accumulation of A2-E in RPE cells interferes with lysosomal functions as exemplified by its inhibitory effect on protein and glycosaminoglycan catabolic pathways.

Inhibition of RPE lysosomal and antioxidant activity by the age pigment lipofuscin.

Lipofuscin has the capacity to reduce the efficacy of the lysosomal and antioxidant systems in RPE cells that may play an important role in retinal ageing and the development of age-related macular degeneration.

Centrophenoxine slows down but does not reverse, lipofuscin accumulation in cultured cells.

It is shown that centrophenoxine at concentrations of 0.25 or 0.5 mM diminishes lipofuscin accumulation within cultured neonatal rat cardiac myocytes when it was constantly present in the culture medium, and the formation of autophagic vacuoles, and ensuing degradation of their contents, are not influenced by centropenoxine.