Cardiac fibrosis, characterized by excessive extracellular matrix accumulation and perpetual fibroblast activation, represents a common pathological endpoint across diverse cardiovascular diseases. Despite its central role in adverse cardiac remodeling and heart failure progression, targeted antifibrotic therapies remain largely elusive. This review synthesizes recent breakthroughs in understanding the molecular and cellular drivers of cardiac fibrosis, highlighting the complex interplay between fibrogenic signaling pathways, immune mechanisms, and extracellular matrix dynamics. We critically evaluate emerging diagnostic modalities from advanced imaging techniques to novel biomarker panels, emphasizing their translational potential and limitations. Current pharmacological approaches achieve only modest antifibrotic effects, whereas emerging targeted therapies such as small-molecule drugs, immunomodulatory agents, and cell-based strategies have shown promising results in preclinical models. The integration of precision medicine approaches with bioengineered platforms represents a paradigm shift in developing personalized antifibrotic interventions. This review provides a comprehensive framework for understanding the translational landscape of cardiac fibrosis and identifies critical gaps that must be addressed to advance effective therapies from bench to bedside.
Trần et al. (2025) studied this question.