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What Goes Wrong with Lon in Ageing?

Kelvin J A Davies1

  • 1University of Southern California, Andrus Gerontology Center of the Davis School of Gerontology, and Division of Molecular & Computational Biology, College of Letters, Arts & Sciences, USA.

Free Radical Biology & Medicine
|October 14, 2015
PubMed
Summary

The human Lon protease degrades damaged mitochondrial proteins. Declining Lon activity with age may contribute to aging and associated diseases, suggesting a role in aging theories.

Area of Science:

  • Molecular Biology
  • Cellular Stress Response
  • Aging Research

Background:

  • The human Lon protease degrades oxidized mitochondrial proteins, preventing aggregation.
  • Lon is a stress-responsive gene induced by various stressors.
  • Lon induction protects cells from oxidative stress damage.

Purpose of the Study:

  • To investigate the role of Lon protease in cellular aging and age-associated diseases.
  • To determine if declining Lon activity contributes to the aging process.
  • To propose Lon's role in the Free Radical Theory of Aging.

Main Methods:

  • Studied Lon protease activity in young, senescent, and aged cells.
  • Utilized stress induction and Lon inhibition (siRNA) in cellular models.

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  • Examined Lon's role in stress response and protection against oxidative damage.
  • Reviewed studies in model organisms (Drosophila, mice) regarding aging and Lon.

    • Main Results:

    • Lon activity declines in senescent and aged cells.
    • Adaptational responses to stress become less effective with age.
    • Studies in flies and mice suggest declining Lon activity is linked to aging.
    • Impaired Lon induction correlates with increased protein damage and mitochondrial dysfunction in aging.

    Conclusions:

    • Declining Lon protease activity may contribute to the aging process and age-associated diseases.
    • Impaired induction of Lon and other stress-responsive genes should be considered in aging theories.
    • Lon protease is a generalized stress-protective enzyme whose decline impacts cellular health during aging.