Single-cell transcriptomics reveal that cardiac fibroblasts transition into distinct functional states, including adaptive CTHRC1+ reparative cells and maladaptive FAP+POSTN+ pathogenic subpopulations.
Cardiac fibrosis is a central feature of heart disease, driven by excessive extracellular matrix (ECM) accumulation and associated with mechanical stiffening, electrical instability, and heart failure. While cardiac fibroblasts (CFs) were historically viewed as a uniform ECM-producing population, lineage tracing and single-cell/spatial transcriptomics reveal substantial fibroblast heterogeneity in healthy myocardium and distinct activation trajectories in disease. This review summarizes fibroblast states in the uninjured heart and the dynamic emergence of specialized fibroblast subpopulations after ischemic injury (myocardial infarction) and during chronic pressure overload. We highlight immune-fibroblast crosstalk as key determinants of fibroblast fate, and discuss how these insights enable precision anti-fibrotic strategies that target pathogenic subtypes while preserving adaptive repair.
Gu et al. (2026) conducted a review in Cardiac fibrosis. Single-cell transcriptomics reveal that cardiac fibroblasts transition into distinct functional states, including adaptive CTHRC1+ reparative cells and maladaptive FAP+POSTN+ pathogenic subpopulations.
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