Abstract
Aging is a complex and integrated gradual deterioration of cellular activities in specific organs of the body, which is associated with increased mortality. This deterioration is the primary risk factor for major human pathologies, including cancer, diabetes, cardiovascular disorders, neurovascular disorders, and neurodegenerative diseases. There are nine tentative hallmarks of aging. In addition, several of these hallmarks are increasingly being associated with acute brain injury conditions. In this review, we consider the genes and their functional pathways involved in brain aging as a means of developing new strategies for therapies targeted to the neuropathological processes themselves, but also as targets for many age-related brain diseases. A single microRNA (miR), which is a short, non-coding RNA species, has the potential for targeting many genes simultaneously and, like practically all other cellular processes, genes associated with many features of brain aging and injury are regulated by miRs. We highlight how certain miRs can mediate deregulation of genes involved in neuroinflammation, acute neuronal injury and chronic neurodegenerative diseases. Finally, we review the recent progress in the development of effective strategies to block specific miR functions and discuss future approaches with the prediction that anti-miR drugs may soon be used in the clinic.
Highlights
Aging is a complex and integrated gradual deterioration of cellular activities in organs of the body that corresponds with increased morbidity and mortality [1]
Human aging is characterized by chronic, low-grade systemic inflammation, which occurs during physiological aging in the absence of overt infection; this phenomenon has been termed as “inflammaging.” [161]
Target genes has provided insights into the molecular mechanisms by which aging processes are regulated at the cell, tissue, organ, and organism level
Summary
Cells continuously encounter various DNA-damaging factors, which give rise to DNA damage throughout life. In silico analysis (Sarkar, unpublished observation) revealed that miR-34a, whose expression is known to be increased in the aging heart and brain, targets XRCC1, FEN1, and UDG. Increased miR-34a expression in the aging mouse heart induces telomere attrition, causing cardiomyocyte cell death and inhibition of myocardial function. In silico analysis (Sarkar, unpublished) revealed that miR-34a targets TRET, and TREF2 genes This downregulation may cause telomere shortening in the aging heart, which is currently associated with cellular senescence in microRNAs in Aging and Disease cardiovascular cells, including cardiomyocytes, vascular endothelial cells, and vascular smooth muscle cells, resulting in cardiovascular diseases. In silico analysis indicates that miR-34a targets the white matter plasticity gene, myelin regulatory factor (Myrf), which is a transcription factor, and the master regulator for myelination within the central nervous system (Sarkar, unpublished). These areas elicit an immune response similar to what occurs in the periphery [93, 95]
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