Cellular senescence refers to the permanent arrest of cell cycle caused by intrinsic and/or extrinsic stressors including oncogene activation, irradiation, DNA damage, oxidative stress, and certain cytokines (including senescence associated secretory phenotype). Cellular senescence is an important factor in aging. Accumulation of senescent cells has been implicated in the causation of various age-related organ disorders, tissue dysfunction, and chronic diseases. It is widely accepted that the biological effects triggered by low-dose radiation (LDR) are different from those caused by high-dose radiation. Experimental evidence suggests that LDR may promote growth and development, enhance longevity, induce embryo production, and delay the progression of chronic diseases. The underlying mechanisms of these effects include modulation of immune response, stimulation of hematopoietic system, antioxidative effect, reduced DNA damage and improved ability for DNA damage repair. In this review, we discuss the possible mechanisms by which LDR prevents senescence and aging from the perspectives of inhibiting cellular senescence and promoting the removal of senescent cells. We review a wide broad of evidence about the beneficial impact of LDR in senescence and aging models (including cardiovascular diseases, neurological diseases, arthritis and osteoporosis, chronic obstructive pulmonary disease and idiopathic pulmonary fibrosis) to highlight the potential value of LDR in preventing aging and age-related diseases. However, there is no consensus on the effect of LDR on human health, and several important aspects require further investigation.
Keywords: Aging; Immune; Low-dose radiation (LDR); Senescence; Senescent cells.
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