Redox theory in progeria

摘要

Scientific investigations, over the past centuries, into longevity and aging have led to the identification of many important hallmarks of aging and the formulation of many hypotheses [1]. For example, the rate-of-living hypothesis, first proposed in 1928, states that longevity may be regarded as a metabolic characteristic [2,3]. This hypothesis may be explained biochemically by the free radical theory of aging, in which oxygen free radicals, called reactive oxygen species (ROS), attack various macromolecules in cells, including proteins, lipids, and deoxyribonucleic acid, causing structural damage to these macromolecules and inducing functional cell senescence [2,3]. Because mitochondria are the main intracellular sources of ROS, the free radical theory was extended to the mitochondrial free radical theory of aging. Moreover, oxidative stress was defined in 1985 as “an imbalance between oxidants and antioxidants in favor of the oxidants, leading to a disruption of redox signaling and control and/or molecular damage” [2,3]. Because oxidative stress has also been observed in the absence of free radicals, the free radical theory of aging was extended, resulting in the formulation of a redox hypothesis of oxidative stress.