LAUSR

Purpose of Review The pathological remodeling of cardiac tissue after injury or disease leads to scar formation. Our knowledge of the role of nonmyocytes, especially fibroblasts, in cardiac injury and repair continues to increase with technological advances in both experimental and clinical studies. Here, we aim to elaborate on cardiac fibroblasts by describing their origins, dynamic cellular states after injury, and heterogeneity in order to understand their role in cardiac injury and repair. Recent Findings With the improvement in genetic lineage tracing technologies and the capability to profile gene expression at the single-cell level, we are beginning to learn that manipulating a specific population of fibroblasts could mitigate severe cardiac fibrosis and promote cardiac repair after injury. Summary Cardiac fibroblasts play an indispensable role in tissue homeostasis and in repair after injury. Activated fibroblasts or myofibroblasts have time-dependent impacts on cardiac fibrosis. Multiple signaling pathways are involved in modulating fibroblast states, resulting in the alteration of fibrosis. Modulating a specific population of cardiac fibroblasts may provide new opportunities for identifying novel treatment options for cardiac fibrosis.