REVIEW: Age-Related Dysfunctions: Evidence and Relationship with Some Risk Factors and Protective Drugs

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G. Libertini^1,a*#, G. Corbi^2,b#, M. Cellurale^3,c, and N. Ferrara^3,4,d

¹Independent researcher, member of the Italian Society for Evolutionary Biology, Italy

²Department of Medicine and Health Sciences, University of Molise, and Italian Society of Gerontology and Geriatrics (SIGG), 86100 Campobasso, Italy

³Department of Translational Medical Sciences, Federico II University of Naples, Naples; Italian Society of Gerontology and Geriatrics (SIGG), Florence, Italy

⁴Istituti Clinici Scientifici Maugeri IRCCS, SpA SB, Telese Terme (BN), Italy

^* To whom correspondence should be addressed.

^# These authors contributed equally to this work.

Received March 16, 2019; Revised August 13, 2019; Accepted August 23, 2019

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The theories interpreting senescence as a phenomenon favored by natural selection require the existence of specific, genetically determined and regulated mechanisms that cause a progressive age-related increase in mortality. The mechanisms defined in the subtelomere–telomere theory suggest that progressive slackening of cell turnover and decline in cellular functions are determined by the subtelomere–telomere–telomerase system, which causes a progressive “atrophic syndrome” in all organs and tissues. If the mechanisms underlying aging-related dysfunctions are similar and having the same origin, it could be hypothesized that equal interventions could produce similar effects. This article reviews the consequences of some factors (diabetes, obesity/dyslipidemia, hypertension, smoking, moderate use and abuse of alcohol) and classes of drugs [statins, angiotensin-converting enzyme (ACE) inhibitors, sartans] in accelerating and anticipating or in counteracting the process of aging. The evidence is compatible with the programmed aging paradigm and the mechanisms defined by the subtelomere–telomere theory but it has no obvious discriminating value against the theories of non-programmed aging paradigm. However, the existence of mechanisms, determined by the subtelomere–telomere–telomerase system and causing a progressive age-related decline in fitness through gradual cell senescence and cell senescence, is not justifiable without an evolutionary motivation. Their existence is expected by the programmed aging paradigm, while is incompatible with the opposite paradigm.

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KEY WORDS: aging, telomere, subtelomere, programmed aging paradigm, non-programmed aging paradigm, risk factors, protective drugs

DOI: 10.1134/S0006297919120034

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