A multi-omics analysis of human fibroblasts overexpressing an <i>Alu</i> transposon reveals widespread disruptions in aging-associated pathways.

ABSTRACT: During aging and cellular senescence, repetitive elements are frequently transcriptionally derepressed across species and cell types. Among these, the most abundant repeats by copy number in the human genome are Alu retrotransposons. Though Alu elements are often studied for their mutagenic potential, there is increasing appreciation for their contributions to other biological functions, including pro-inflammatory signaling and mitochondrial dysfunction. However, a comprehensive analysis of Alu-driven molecular changes remains to be conducted, and Alu's potential contributions to aging features remain incompletely characterized. Here, we show that overexpression of an AluJb transposon in human primary IMR-90 fibroblasts leads to large-scale alterations ac

SUBMITTER: Bravo JI 

PROVIDER: S-EPMC12338678 | biostudies-literature | 2025 Oct

REPOSITORIES: biostudies-literature