Introduction: Aging researches have experienced an unprecedented advance over recent years. The comprehension of process leading to age-associated alterations for the development of new treatments for age-associated diseases, such as cancer, diabetes, Alzheimer and cardiovascular accidents but also to encourage healthy gain of years with high standard of quality of life is encouraged. It is widely considered that the accumulation of molecular and cellular damage influenced by reactive oxygen species producing oxidation might orchestrate the progressive loss of control over biological homeostasis and the functional impairment typical of aged tissues.

Objective: The overall aim of this work is review the general and clinical aspects of aging and connects biological at molecular, cellular and organism levels.

Materials and methods: Through general overview of findings reported in consulted literature (132 valid documents-53 selected) is sustained how resulting oxidative stress-redox disruption signal took part in the mechanisms of ageing physiology and physiopathology.

Results: Findings related to aging controlled, at least to some extent, by genetic pathways and biochemical processes conserved in evolution is discussed and integrates to common denominators of aging in different organisms, with special emphasis on mammalian aging. The aspects considered in overview are: genomic instability, telomere attrition, epigenetic alterations, loss of proteostasis, deregulated nutrient sensing, mitochondrial dysfunction, cellular senescence, stem cell exhaustion, and altered intercellular communication.

Conclusions: Based on the revisited aging associated redox mechanisms causing damage, the compensatory responses leading to homeostasis reestablishment and the interconnection between them are analyzed and explored with the final goal of identifying pharmaceutical targets to improve human health during aging, with minimal side effects.