Despite advances in understanding cardiac fibrosis, current therapies cannot reverse established fibrosis, highlighting a major gap in targeted antifibrotic treatments.
Cardiac fibrosis, characterized by excessive extracellular matrix deposition, contributes to heart failure, arrhythmias, and myocardial dysfunction. Despite advances in understanding its mechanisms, targeted antifibrotic therapies remain limited. This review examines the causes, molecular mechanisms, diagnostic approaches, and therapeutic strategies for cardiac fibrosis. A systematic review of peer-reviewed studies was conducted, focusing on the etiology, diagnosis, treatment, and prognosis of cardiac fibrosis with no specific timeframe. The condition is driven by fibroblast activation, inflammatory pathways, and mechanical stress, with key contributing factors including ischemic heart disease, hypertension, diabetes, and aging. Diagnostic tools such as cardiac magnetic resonance imaging with T1 mapping and biomarkers play a crucial role, with natriuretic peptides offering both diagnostic and prognostic value. Galectin-3 has also shown promise as a prognostic marker. Current therapies, including RAAS inhibitors and beta-blockers, help prevent fibrosis progression but do not reverse established fibrosis. Emerging strategies such as plant-based compounds, gene therapy, fibroblast-targeting vaccines, and stem cell reprogramming show potential in preclinical studies. However, cardiac fibrosis remains a major driver of heart disease progression, and existing treatments remain limited. Major gaps include the lack of validated antifibrotic agents and challenges in translating preclinical findings into clinical applications. Further research is essential to develop effective targeted interventions.
BaniHani et al. (Thu,) studied this question.