Upregulation of miR-29 Appears to Promote Degenerative Aging
Researchers have discovered that the upregulation of a specific microRNA, miR-29, is associated with the aging process. When miR-29 expression is artificially increased, it leads to aging-like disruptions in metabolism and premature mortality. Despite the increase in miR-29 expression with age, the underlying reasons remain unclear, with current research mainly focusing on the downstream effects. Aging involves numerous maladaptive changes in gene expression, with some potentially more significant than others. The potential impact of blocking certain age-related gene expression changes with suitable drug interventions on extending healthy lifespan is an area that requires further investigation.
Aging is a complex process involving molecular changes, and the role of a single microRNA (miRNA) in driving aging is still not fully understood. MiR-29 is one such miRNA that is upregulated during normal and premature aging, and is predicted to drive aging-related gene expression changes. Studies have shown that reducing miR-29 levels extends the lifespan of progeria model mice, indicating the functional importance of miR-29 in accelerated aging models.
To investigate if miR-29 alone can promote aging-related effects, researchers created mice with conditional overexpression of miR-29 (miR-29TG). Overexpression of miR-29 resulted in various aging-related phenotypes and premature mortality. Transcriptomic analysis of both young miR-29TG mice and old wild type mice revealed common downregulation of genes related to extracellular matrix organization and fatty acid metabolism, as well as upregulation of genes associated with inflammation pathways. These findings underscore the critical role of miR-29 in regulating a gene expression profile that drives aging-related traits.
Link: https://doi.org/10.1038/s42003-024-06735-z
