Introduction to Special Issue on 'Physiological and PA Evolutionary Mechanisms of Aging'.
What are the structural components and physiological mechanisms determining the aging process? Can the different mechanisms described in aging biology converge into a core of coordinated aging effectors? Why some human beings, for instance, can reach 115-122 years of age while rats can live at best a maximum of 4 years? Can the aging rate be modified? How much can human lifespan be extended? Is aging a programmed or non-programmed process? This special issue includes invited articles to explore the physiological mechanisms of aging, and both classical and updated hypotheses on the evolutionary meaning of aging. Breakthroughs in aging-related research are currently unveiling longevity factors highly conserved during evolution of animal species and are discovering details on how and why molecular and cellular processes decline during physiologically normal aging. Investigations in model organisms and humans are uncovering potential approaches to extend not only mean individual survival but also species maximum (from here on) longevity. Experimental Gerontology presents this Special Issue (SI) highlighting recent advances in the mechanistic understanding of longevity, aging and interventions that extend lifespan. This SI includes invited articles to address most of the reasonably well known physiological mechanisms of aging, and tries to evaluate the available evidence supporting or not the different opposed hypotheses on the biological evolution of aging, why aging exists at all?. The SI is composed of ten peer reviewed invited reviews and primary research articles, covering basic concepts on aging biology and species longevity, with a special specific focus on mitochondrial function, mitROS production (mitROSp), mitDNA damage and caloric restriction; autophagy; the role of dietary antioxidants; the only drug that has consistently demonstrated (ITP/NIA/NIH program performed at three independent laboratories) that increases longevity in mammals over that of normal controls: rapamycin; heterochronic parabiosis; secondary inflammaging; the role of epigenetics in the control of a cellular nuclear aging program, and the hypothetical existence of peripheral and central aging clocks.
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