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Arginase-II Deficiency Extends Lifespan in Mice
Yuyan Xiong1, Gautham Yepuri1, Jean-Pierre Montani1,2
1Division of Physiology, Cardiovascular and Aging Research, Department of Medicine, University of FribourgFribourg, Switzerland.
Frontiers in Physiology
|September 26, 2017
Summary
Mitochondrial arginase type II (Arg-II) deficiency significantly extends lifespan in mice, particularly females. This suggests Arg-II is a key factor in aging and a potential target for longevity interventions.
Area of Science:
- Gerontology
- Mitochondrial Biology
- Molecular Aging
Background:
- Mitochondrial arginase type II (Arg-II) interacts with S6K1 and p66Shc, promoting cellular senescence, apoptosis, and inflammation.
- The effect of Arg-II on organismal lifespan remains largely unknown.
Purpose of the Study:
- To investigate the impact of Arg-II deficiency on mouse lifespan.
- To explore the underlying molecular mechanisms and gender-specific differences.
Main Methods:
- Lifespan analysis of Arg-II gene-deficient (Arg-II-/-) mice compared to wild-type (WT) controls.
- Measurement of aging markers (p16INK4a) and signaling pathways (S6K1, p66Shc) in various tissues.
- Analysis of gender-specific differences in Arg-II expression and its effects.
Main Results:
- Arg-II-/- mice exhibited significantly extended lifespan compared to WT mice, with a more pronounced effect in females.
- Arg-II deficiency reduced p16INK4a levels in old female mice.
- Age-associated increases in S6K1 and p66Shc signaling were attenuated in female Arg-II-/- mice, while only p66Shc was reduced in males.
Conclusions:
- Arg-II plays a significant role in accelerating aging in mice.
- Genetic disruption of Arg-II extends lifespan, predominantly in females, by inhibiting S6K1, p66Shc, and p16INK4a.
- Arg-II is a potential therapeutic target for decelerating aging and treating age-related diseases.
