In addition, several of the pathologies associated with aging, such as atherosclerosis and inflammation, involve uncontrolled cellular overgrowth or hyperactivity ( Blagosklonny, 2008). Therefore, cancer and aging can be regarded as two different manifestations of the same underlying process, namely, the accumulation of cellular damage. Concomitantly, cellular damage may occasionally provide aberrant advantages to certain cells, which can eventually produce cancer. The time-dependent accumulation of cellular damage is widely considered the general cause of aging ( Gems and Partridge, 2013 Kirkwood, 2005 Vijg and Campisi, 2008). At a deeper level, however, cancer and aging may share common origins. This categorization has helped to conceptualize the essence of cancer and its underlying mechanisms.Īt first sight, cancer and aging may seem opposite processes: cancer is the consequence of an aberrant gain of cellular fitness, while aging is characterized by a loss of fitness. The cancer field gained major momentum in 2000 with the publication of a landmark paper that enumerated six hallmarks of cancer ( Hanahan and Weinberg, 2000), and that has been recently expanded to ten hallmarks ( Hanahan and Weinberg, 2011). The current situation of aging research exhibits many parallels with that of cancer research in previous decades. Nowadays, aging is subjected to scientific scrutiny based on the ever-expanding knowledge of the molecular and cellular bases of life and disease. However, it is only 30 years since a new era in aging research was inaugurated after the isolation of the first long-lived strains in Caenorhabditis elegans ( Klass, 1983). A major challenge is to dissect the interconnectedness between the candidate hallmarks and their relative contribution to aging, with the final goal of identifying pharmaceutical targets to improve human health during aging with minimal side-effects.Īging, which we broadly define as the time-dependent functional decline that affects most living organisms, has attracted curiosity and excited imagination throughout the history of humankind. These hallmarks are: genomic instability, telomere attrition, epigenetic alterations, loss of proteostasis, deregulated nutrient-sensing, mitochondrial dysfunction, cellular senescence, stem cell exhaustion, and altered intercellular communication. This review enumerates nine tentative hallmarks that represent common denominators of aging in different organisms, with special emphasis on mammalian aging. Aging research has experienced an unprecedented advance over recent years, particularly with the discovery that the rate of aging is controlled, at least to some extent, by genetic pathways and biochemical processes conserved in evolution. This deterioration is the primary risk factor for major human pathologies including cancer, diabetes, cardiovascular disorders, and neurodegenerative diseases. Aging is characterized by a progressive loss of physiological integrity, leading to impaired function and increased vulnerability to death.
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