Available online 19 March 2024, 107635

Cardiac fibrosis continues to play an important role in driving adverse clinical outcomes for a growing number of patients worldwide.

Various cellular and molecular pathways have been implicated in the pathogenesis of cardiac fibrosis.

Recent work has revealed that the local immune microenvironment may have a critical role underlying the progression of cardiac fibrosis.

Stem cell therapy for treating cardiac fibrosis has been fraught with challenges, but ongoing studies suggest a more precise approach may have benefits in blunting the progression of fibrotic processes in the heart.

Cardiac fibrosis is a significant contributor to heart failure, a condition that continues to affect a growing number of patients worldwide. Various cardiovascular comorbidities can exacerbate cardiac fibrosis. While fibroblasts are believed to be the primary cell type underlying fibrosis, recent and emerging data suggest that other cell types can also potentiate or expedite fibrotic processes. Over the past few decades, clinicians have developed therapeutics that can blunt the development and progression of cardiac fibrosis. While these strategies have yielded positive results, overall clinical outcomes for patients suffering from heart failure continue to be dire. Herein, we overview the molecular and cellular mechanisms underlying cardiac tissue fibrosis. To do so, we establish the known mechanisms that drive fibrosis in the heart, outline the diagnostic tools available, and summarize the treatment options used in contemporary clinical practice. Finally, we underscore the critical role the immune microenvironment plays in the pathogenesis of cardiac fibrosis.

Cardiac fibrosis

remodelling

repair

heart failure

therapeutics

The authors confirm that the data presented herein are in peer-reviewed publications indexed on Medline/PubMed.

© 2024 The Author(s). Published by Elsevier Inc.