The biochemistry and cell biology of aging: metabolic regulation through mitochondrial signaling

Cellular and organ metabolism affects organismal lifespan. Aging is characterized by increased risks for metabolic disorders, with age-associated degenerative diseases exhibiting varying degrees of mitochondrial dysfunction. The traditional view of the role of mitochondria generated reactive oxygen...

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Bibliographic Details
Published in:American journal of physiology: endocrinology and metabolism 2014-03, Vol.306 (6), p.E581-E591
Main Authors: Long, Yun Chau, Tan, Theresa May Chin, Takao, Inoue, Tang, Bor Luen
Format: Article
Language:English
Subjects:
Aging
Aging - metabolism
Animals
Biochemistry
Cellular biology
Endocrinology
Epigenesis, Genetic
Humans
Longevity
Metabolic Diseases - etiology
Metabolic Diseases - metabolism
Metabolic Diseases - prevention & control
Metabolism
Mitochondria
Mitochondria - metabolism
Models, Biological
Oxidative Stress
Signal Transduction
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Summary:Cellular and organ metabolism affects organismal lifespan. Aging is characterized by increased risks for metabolic disorders, with age-associated degenerative diseases exhibiting varying degrees of mitochondrial dysfunction. The traditional view of the role of mitochondria generated reactive oxygen species (ROS) in cellular aging, assumed to be causative and simply detrimental for a long time now, is in need of reassessment. While there is little doubt that high levels of ROS are detrimental, mounting evidence points toward a lifespan extension effect exerted by mild to moderate ROS elevation. Dietary caloric restriction, inhibition of insulin-like growth factor-I signaling, and inhibition of the nutrient-sensing mechanistic target of rapamycin are robust longevity-promoting interventions. All of these appear to elicit mitochondrial retrograde signaling processes (defined as signaling from the mitochondria to the rest of the cell, for example, the mitochondrial unfolded protein response, or UPR(mt)). The effects of mitochondrial retrograde signaling may even spread to other cells/tissues in a noncell autonomous manner by yet unidentified signaling mediators. Multiple recent publications support the notion that an evolutionarily conserved, mitochondria-initiated signaling is central to the genetic and epigenetic regulation of cellular aging and organismal lifespan.
ISSN:0193-1849
1522-1555
DOI:10.1152/ajpendo.00665.2013