Abstract
The problem of human exposure to ionizing radiation has attracted increasing attention in various scientific fields. Recently, a substantial amount of data has been collected on the age-related risks associated with radiation exposure, which has enabled researchers to uncover the relationship between ionizing radiation and cellular senescence. This has led to the search for cellular targets of radiation, with mitochondria being one of the identified targets. Ionizing radiation causes mitochondrial dysfunction and the emergence of a characteristic age-related phenotype in cells, including increased ROS production, SASP development, changes in the epigenetic profile, and genomic instability. Mitochondrial dysfunction is often underestimated as a crucial hallmark of cellular senescence, and its underlying mechanisms are extensive and complex. In particular, mitochondrial miRNAs (mitomiRs) that regulate mitochondrial gene expression, and consequently, the function and dynamics of the organelles themselves, are of particular interest. Considering that mitomiRs are highly sensitive to even minor disturbances arising from irradiation, resulting in significant changes in their expression, they may serve as promising biomarkers of radiation exposure. In this review, we examine the evidence supporting the key role of mitomiRs in radiation-induced cellular senescence and integrate the latest knowledge on the underlying molecular mechanisms of this interaction.