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Endothelial Cells retain inflammatory memory through chromatin remodeling [ATAC]

GSE301784 Mus musculus Genome binding/occupancy profiling by high throughput sequencing 12 samples 2025/11/06 GPL34475
Summary
Sepsis survivors exhibit long-term endothelial dysfunction, increasing susceptibility to secondary infections such as pneumonia. To investigate the molecular basis of endothelial inflammatory memory, we performed transcriptomic profiling of lung and kidney endothelial cells isolated from a murine two-hit sepsis model. This model incorporates cecal ligation and puncture (CLP) as the primary inflammatory event, followed by a secondary intranasal challenge with Streptococcus pneumoniae.
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