How increased oxidative stress promotes longevity and metabolic health: The concept of mitochondrial hormesis (mitohormesis)

@article{Ristow2010HowIO,
  title={How increased oxidative stress promotes longevity and metabolic health: The concept of mitochondrial hormesis (mitohormesis)},
  author={Michael Ristow and Kim Zarse},
  journal={Experimental Gerontology},
  year={2010},
  volume={45},
  pages={410-418}
}
Recent evidence suggests that calorie restriction and specifically reduced glucose metabolism induces mitochondrial metabolism to extend life span in various model organisms, including Saccharomyces cerevisiae, Drosophila melanogaster, Caenorhabditis elegans and possibly mice. In conflict with Harman's free radical theory of aging (FRTA), these effects may be due to increased formation of reactive oxygen species (ROS) within the mitochondria causing an adaptive response that culminates in… Expand
Effects of Caloric Restriction on Cardiac Oxidative Stress and Mitochondrial Bioenergetics: Potential Role of Cardiac Sirtuins
  • K. Shinmura
  • Biology, Medicine
  • Oxidative medicine and cellular longevity
  • 2013
TLDR
It is speculated that cardiac sirtuins attenuate the accumulation of oxidative damage associated with age by modifying specific mitochondrial proteins posttranscriptionally, and the distinct role of each sirtuin in the heart subjected to caloric restriction should be clarified to translate sirtin biology into clinical practice. Expand
Nutritional Ketosis and Mitohormesis: Potential Implications for Mitochondrial Function and Human Health
TLDR
The evidence supporting enhancement of mitochondrial function and endogenous antioxidant defense in response to nutritional ketosis is described, as well as the potential mechanisms leading to these adaptations. Expand
NRF2 and the Phase II Response in Acute Stress Resistance Induced by Dietary Restriction.
TLDR
A review of the potential role of the redox-sensing transcription factor NF-E2-related factor 2 (NRF2) and its control of the evolutionarily conserved antioxidant/redox cycling and detoxification systems, collectively known as the Phase II response, in the adaptive response to DR. Expand
Mitohormesis and metabolic health: The interplay between ROS, cAMP and sirtuins.
TLDR
Reversible phosphorylation downstream the cyclic AMP (cAMP) signaling cascade and deacetylation mediated by sirtuins are recognized as major mitochondrial regulators. Expand
The biochemistry and cell biology of aging: metabolic regulation through mitochondrial signaling.
TLDR
mounting evidence points toward a lifespan extension effect exerted by mild to moderate ROS elevation, and the notion that an evolutionarily conserved, mitochondria-initiated signaling is central to the genetic and epigenetic regulation of cellular aging and organismal lifespan. Expand
Mitohormesis in muscle cells: a morphological, molecular, and proteomic approach.
TLDR
Mitochondrial remodeling in response to different degrees of oxidative insults induced in vitro in myocytes and in vivo in skeletal muscle is described, focusing on the potential application of a combined morphological and biochemical approach. Expand
Mitochondrial oxidative stress in aging and healthspan
TLDR
Evidence supporting the role of mitochondrial oxidative stress, mitochondrial damage and dysfunction in aging and healthspan, including cardiac aging, age-dependent cardiovascular diseases, skeletal muscle aging, neurodegenerative diseases, insulin resistance and diabetes as well as age-related cancers is reviewed. Expand
Mitochondrial Hormesis links nutrient restriction to improved metabolism in fat cell
TLDR
It is shown that white and beige adipocytes, as well as mouse epididymal and subcutaneous adipose depots, respond to nutrient scarcity by acquiring a brown-like phenotype, highlighting an unusual white/beige fat cell response to nutrient availability highlighting another health-promoting mechanism of fasting. Expand
Mitochondrial-Targeted Catalase: Extended Longevity and the Roles in Various Disease Models.
TLDR
The laboratory developed mice-overexpressing catalase targeted to mitochondria, peroxisomes, or the nucleus (nCAT) in order to investigate the role of hydrogen peroxide in different subcellular compartments in aging and age-related diseases and the potential pleiotropic, or adverse effects of mCAT are discussed. Expand
Cellular Stress Responses, Mitostress and Carnitine Insufficiencies as Critical Determinants in Aging and Neurodegenerative Disorders: Role of Hormesis and Vitagenes
TLDR
How hormetic dose responses are mediated for endogenous cellular defense pathways are described, including the possible signaling mechanisms by which the carnitine system modulates signal transduction cascades that confer cytoprotection against chronic degenerative damage associated to aging and neurodegenerative disorders are described. Expand
...
1
2
3
4
5
...

References

SHOWING 1-10 OF 243 REFERENCES
Glucose restriction extends Caenorhabditis elegans life span by inducing mitochondrial respiration and increasing oxidative stress.
TLDR
It is indicated that glucose restriction promotes mitochondrial metabolism, causing increased ROS formation and cumulating in hormetic extension of life span, questioning current treatments of type 2 diabetes as well as the widespread use of antioxidant supplements. Expand
Reversal of the Mitochondrial Phenotype and Slow Development of Oxidative Biomarkers of Aging in Long-lived Mclk1+/− Mice*
TLDR
This study provides for a unique vertebrate model in which an initial alteration in a specific mitochondrial function is linked to long term beneficial effects on biomarkers of aging and provides for new evidence which indicates that mitochondrial oxidative stress is not causal to aging. Expand
Calorie restriction induces mitochondrial biogenesis and bioenergetic efficiency.
TLDR
Calorie restriction can induce a peroxisome proliferation-activated receptor coactivator 1 alpha-dependent increase in mitochondria capable of efficient and balanced bioenergetics to reduce oxidative stress and attenuate age-dependent endogenous oxidative damage. Expand
Caloric restriction augments ROS defense in S. cerevisiae, by a Sir2p independent mechanism
TLDR
Evidence is provided that not only oxygen consumption but ROS production is enhanced in the calorie restricted condition and Sir2, a potential effector of CR response in the activation of scavenging enzymes are activated by a Sir2 independent manner. Expand
Sublethal mitochondrial stress with an attendant stoichiometric augmentation of reactive oxygen species may precipitate many of the beneficial alterations in cellular physiology produced by caloric restriction, intermittent fasting, exercise and dietary phytonutrients: "Mitohormesis" for health and
TLDR
It may be necessary for the research community and the practicing clinician to engender a more sanguine perspective on organelle level physiology, as it is now plausible that such entities have an evolutionarily orchestrated capacity to self-regulate that may be pathologically disturbed by overzealous use of antioxidants, particularly in the healthy. Expand
The coordination of nuclear and mitochondrial communication during aging and calorie restriction
TLDR
This review will focus on PGC-1alpha, SIRT1, AMPK and mTOR and discuss how these proteins regulate mitochondrial function and their potential involvement in aging, calorie restriction and age-related disease. Expand
Defective Mitochondrial Gene Expression Results in Reactive Oxygen Species-Mediated Inhibition of Respiration and Reduction of Yeast Life Span
TLDR
The results provide compelling evidence for the “vicious cycle” of mitochondrial ROS production and lead us to propose that the amount of ROS generated depends on the precise nature of the mitochondrial gene expression defect and initiates a downward spiral of oxidative stress only if a critical threshold is crossed. Expand
Minireview: the role of oxidative stress in relation to caloric restriction and longevity.
TLDR
Recent reports of caloric restriction and longevity are reviewed, focusing on mitochondrial oxidative stress and the proposed mechanisms leading to an extended longevity in calorie-restricted animals. Expand
The mitochondrial theory of aging: Insight from transgenic and knockout mouse models
TLDR
The goal of this review is to provide a concise summary of recent studies using transgenic and knockout mouse models with altered expression of mitochondrial antioxidant enzymes that do not support a clear role for mitochondrial oxidative stress or a vicious cycle of oxidative damage in the determination of lifespan in mice. Expand
Reduced TOR signaling extends chronological life span via increased respiration and upregulation of mitochondrial gene expression.
TLDR
It is proposed that inhibition of TOR signaling causes derepression of respiration during growth in glucose and that the subsequent increase in mitochondrial oxygen consumption limits intracellular oxygen and ROS-mediated damage during glycolytic growth, leading to lower cellular ROS and extension of chronological life span. Expand
...
1
2
3
4
5
...