The Interplay between Mitochondria, MitomiRs, Radiation, and Age-Related Diseases:Prospects for Research

Abstract

Aging is a complex biological process characterized by the gradual decline of cellular, tissue, and organ functions, ultimately contributing to the onset of age-associated diseases such as cardiovascular disorders, neurodegenerative conditions, and metabolic syndromes. Among the environmental factors influencing aging, radiation, particularly ionizing radiation, has emerged as a significant contributor to agerelated deterioration. Despite advancements in understanding, the precise mechanisms by which radiation accelerates aging remain incompletely elucidated. Recent research underscores the pivotal role of mitochondria and microRNAs (miRNAs), specifically mitomiRs, in mediating the effects of radiation on aging. Mitochondria, as the cellular energy powerhouses,
are central to maintaining metabolic homeostasis and regulating cellular responses to stress. Radiation-induced alterations in miRNA expression profiles can disrupt these processes by impairing mitochondrial dynamics,
biogenesis, and mitophagy. Additionally, radiation directly damages mitochondrial DNA (mtDNA) and mRNA, further compromising mitochondrial function. These changes not only accelerate the aging process but also increase susceptibility to age-associated diseases.
Age-related diseases, such as Alzheimer’s disease, diabetes, and cancer, are strongly linked to mitochondrial dysfunction. Radiation exacerbates these conditions by amplifying oxidative stress, triggering inflammatory
pathways, and impairing mitochondrial quality control mechanisms. Dysregulated mitomiRs play a dual role, acting both as mediators of damage and as potential biomarkers for identifying radiation-induced aging and disease progression. This review consolidates existing evidence on the intricate interplay between radiation, miRNAs, mitochondria, and age-related diseases. It explores how radiation influences miRNA expression, mitochondrial health, and their combined effects on cellular metabolism and systemic aging. Understanding these interactions
is crucial for identifying molecular targets and developing innovative strategies to mitigate radiation-induced damage. Novel therapeutic approaches, such as targeting key mitomiRs or enhancing mitochondrial resilience, hold promise for reducing the impact of radiation on aging and age-associated diseases, ultimately improving
health outcomes in affected populations.