Fig. 6.

HNRNPA2B1 marks a pro-inflammatory macrophage state and amplifies MDK/ITGB2-centered crosstalk. (A) Correlation of m⁶A regulators with macrophage functional signatures. (B) Scatter plots showing HNRNPA2B1 expression versus chemotaxis, activation, and migration pathway scores. (C) Violin plots showing decreased IFNGR1 and TRIB1 in HNRNPA2B1-high macrophages. (D) Volcano plot showing differential expression between HNRNPA2B1-high and -low macrophages. (E) GO enrichment of HNRNPA2B1-high macrophages. (F) GSEA enrichment plots of macrophage activation and defense-response terms. (G) Spatial feature plots of the cell type, HNRNPA2B1, and pathway enrichment scores in IPF tissue sections. (H) hdWGCNA turquoise module network of HNRNPA2B1 co-expressed genes. (I) Module–trait correlation heatmap linking turquoise module to inflammatory functions. (J) Cell–cell interaction networks in HNRNPA2B1-high vs. -low macrophages. (K) Overall pathway strength comparison for key signaling routes. (L) Chord diagram of MDK signaling (all senders) in the high state. (M) Upregulated MDK signaling partners in HNRNPA2B1-high. (N) Dot-plot of selected ligand–receptor pairs across sender–receiver lineages; color = communication probability; dot size = significance. (O) Expression distributions (high vs. low) for MDK, ITGB2, ICAM1, PECAM1; significance indicated