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Abstract Cardiac fibrosis is a major contributor to the development and progression of heart failure. It involves an aberrant deposition of extracellular matrix components, leading to impaired mechanical and electrical function of the heart. Despite its clinical importance, effective anti-fibrotic treatments remain elusive, in part due to limited insight into the molecular and cellular processes that distinguish transient from sustained fibrotic responses. Central to these processes are fibroblasts, structurally supportive yet functionally diverse stromal cells that regulate tissue architecture, cell signalling, and immune responses. Recent technological advances, including lineage tracing models and single-cell omics, have begun to unravel the complexity of fibroblast populations within the heart. These approaches have identified distinct fibroblast states and highlighted their dynamic roles in both maintaining homeostasis and driving pathological remodelling. This review examines the evolving understanding of fibroblast biology in the context of myocardial fibrosis, emphasizing their contributions to inflammation and extracellular matrix dysregulation and their interactions with cardiomyocytes and endothelial cells. Finally, emerging therapeutic avenues aimed at selectively altering fibroblast activity and mechanosensitive therapies are highlighted.
Linthout et al. (Tue,) studied this question.