Inflammation and fibrosis are linked to organ dysfunction, yet the cross-talk between immune cells and fibroblasts is poorly understood. Two studies in Nature investigate the interactions between these cells in the context of heart disease.

Amrute et al. established a ‘multiomic map’ of healthy, acutely infarcted and chronically diseased human hearts and used in vivo lineage tracing to define the development of disease-associated fibroblasts. Using mouse models of cardiac injury that closely recapitulate fibroblast trajectories in human disease, as well as spatial transcriptomics and cell-specific deletion of IL-1β or IL-1R, the authors demonstrate a causal link between IL-1β production by CCR2+ monocyte-derived macrophages and cardiac fibrosis in vivo.