A cardiac fibroblast-enriched micropeptide regulates inflammation

Knockdown of IAMP resulted in significant alterations in the transcriptome. Upon cross-analysis of the transcriptomic changes induced by the two siRNAs, we identified 190 genes that were commonly upregulated and 342 genes that were commonly downregulated in both datasets. KEGG enrichment analysis of these differentially expressed genes revealed that IAMP knockdown led to the upregulation of genes associated with inflammation-related pathways, such as the TNF and IL-17 signaling pathways. Collectively, these data suggest that IAMP functions as an anti-inflammatory factor in cardiac fibroblasts. Overall design: RNA-seq of adult mouse cardiac fibroblasts treated with IAMP siRNA and stimulated with IL-17 or TGF-ß.