Focus on the Contribution of Oxidative Stress in Skin Aging

Abstract

Skin aging is one of the most evident signs of human aging. Modification of the skin during the life span is characterized by fine lines and wrinkling, loss of elasticity and volume, laxity, rough-textured appearance, and pallor. In contrast, photoaged skin is associated with uneven pigmentation (age spot) and is markedly wrinkled. At the cellular and molecular level, it consists of multiple interconnected processes based on biochemical reactions, genetic programs, and occurrence of external stimulation. The principal cellular perturbation in the skin driving senescence is the alteration of oxidative balance. In chronological aging, reactive oxygen species (ROS) are produced mainly through cellular oxidative metabolism during adenosine triphosphate (ATP) generation from glucose and mitochondrial dysfunction, whereas in extrinsic aging, loss of redox equilibrium is caused by environmental factors, such as ultraviolet radiation, pollution, cigarette smoking, and inadequate nutrition. During the aging process, oxidative stress is attributed to both augmented ROS production and reduced levels of enzymatic and non-enzymatic protectors. Apart from the evident appearance of structural change, throughout aging, the skin gradually loses its natural functional characteristics and regenerative potential. With aging, the skin immune system also undergoes functional senescence manifested as a reduced ability to counteract infections and augmented frequency of autoimmune and neoplastic diseases. This review proposes an update on the role of oxidative stress in the appearance of the clinical manifestation of skin aging, as well as of the molecular mechanisms that underline this natural phenomenon sometimes accelerated by external factors.

Efficacy and Safety of Oral Green Tea Preparations in Skin Ailments: A Systematic Review of Clinical Studies

“…Regarding mechanisms accounting for photoaging, UV irradiation is known to generate reactive oxygen species (ROS), leading to marked oxidative stress, which impairs the skin functional and regenerative potential. Moreover, activation of photoaging triggers cellular senescence and inflammation, a condition known as inflammaging, and progressively suppresses the skin immune system, increasing susceptibility to infection, degenerative processes, and cancer [ 42 , 43 ]. Molecular targets, including epidermal growth factor (EGF), keratinocyte growth factor, tumor necrosis factor (TNF)-α, and interleukin (IL)-1, are activated by UV radiation, thus, stimulating the transcription factor AP-1, which blocks the synthesis of collagen, while promoting transcription of matrix metalloproteinase (MMP) genes, which in turn triggers imperfect tissue repair and dermal damage [ 44 ].…”

Puerariae lobatae radix protects against UVB-induced skin aging via antagonism of REV-ERBα in mice

“…Moreover, we have observed that PLR treatment (topical application) of mice with UVB-induced photoaging led to increased skin expression of BMAL1 (an aging suppressor) and major antioxidant enzymes, as well as a decreased ROS level. The literature has established that ROS plays a critical role in skin damage and aging caused by UV radiation ( Papaccio et al, 2022 ). UV-generated ROS leads to oxidative stress in the skin and thus to various cellular changes such as an increase in MMPs expression, enhanced collagen degradation and impaired collagen synthesis, which reflect major aspects of skin aging ( Kim et al, 2018 ).…”

“…Although the etiologies of premature skin aging (or photoaging) are not fully elucidated, several contributing factors have been identified, including oxidative stress [i.e., formation of reactive oxygen species (ROS)], mutations of mitochondrial DNA, and shortening of telomeres ( Beani, 2014 ; Papaccio et al, 2022 ; Son et al, 2022 ). Notably, ROS exerts a critical role in photoaging.…”

Post-Translational Modifications Evoked by Reactive Carbonyl Species in Ultraviolet-A-Exposed Skin: Implication in Fibroblast Senescence and Skin Photoaging

“…As recently reviewed by Bernerd et al [ 37 ] and Papaccio et al [ 58 ], chronic UV exposure promotes protein oxidation and carbonylation in the epidermis and dermis, and the accumulation of oxidatively modified and damaged proteins. RCS-adducts are detected in human skin biopsies, in keratinocytes, fibroblasts [ 59 , 60 ] and ECM [ 61 ].…”

“…ECM components (collagen, elastin, glycosaminoglycans), are primary targets of oxidative and carbonyl attack during photoaging [ 58 ]. Zucchi et al recently reported that carbonylated proteins are formed on the connective tissue in the dermis from sun-exposed human skin, specifically MDA-adduct deposits, which may accumulate on collagen [ 44 ].…”