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.
