ArticleMolecular therapy. Nucleic acids2026
Focal ischemia induces genome-wide accumulation of R-loops in the brain.
Article in Molecular therapy. Nucleic acids, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Ischemic stroke induces rapid changes in transcriptional regulatory mechanisms across diverse genomic regions of the brain. These alterations fine-tune gene expression patterns to orchestrate post-stroke pathological responses. Precise control of these processes is critical for limiting brain damage and facilitating long-term neurological recovery. During transcription, RNA can hybridize with the DNA template to form three-stranded RNA:DNA hybrids, termed R-loops. Accumulation of R-loops leads to altered transcriptional fidelity, DNA damage, and genomic instability in several pathological conditions. We currently evaluated the effect of stroke on R-loops in mice subjected to transient focal ischemia. Focal ischemia significantly induced R-loop accumulation and DNA damage in the peri-infarct cortex compared with sham. Immunoprecipitated RNA:DNA hybrids sequencing showed strand and site-specific accumulation of R-loops across the genome, with increased R-loops signal at long-noncoding RNA-associated genomic regions. Gene ontology analysis of genes associated with significantly altered R-loops indicated that they regulate several biological functions, including action potential, axonogenesis, apoptosis, chromatin remodeling, dendrite morphogenesis, and synapse organization, which play a significant role in functional recovery after stroke. Overall, our results indicated a potential role of R-loops in modulating ischemic stroke pathophysiology. Targeting R-loops might be a promising strategy to improve post-stroke recovery.
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