Key result
Targeted anti-fibrotic therapies show promise in reducing fibrotic biomarkers in human cardiac fibrosis, though their clinical importance and impact on outcomes remain to be established.
Why the study?
Cardiac fibrosis is a common pathological feature across diverse cardiovascular diseases, prompting a review of recent advances in its translational biology, assessment, and therapeutic targeting.
This review synthesizes recent advances in the translational biology of human cardiac fibrosis, including insights from single-cell studies, genetics, imaging, biomarkers, and emerging anti-fibrotic therapies.
Clinicians should await outcome trials before considering targeted anti-fibrotics; leaves open their impact on hard endpoints in cardiac fibrosis.
Cardiac fibrosis is a pathological process that arises as a compensatory response to injury or mechanical stress and is a common feature across diverse cardiovascular diseases. Here, we review recent advances in the translational biology of human cardiac fibrosis, highlighting insights from single-cell studies of human cardiac fibroblasts and genetic analyses of fibrotic phenotypes using cardiac imaging. We discuss the heterogeneity and origins of cardiac fibroblasts, the role of immune–fibroblast cross-talk in fibrogenesis, and the utility of imaging and circulating biomarkers for assessing fibrotic burden. Existing antihypertensive therapies have demonstrated direct effects on cardiac fibroblasts and tissue-level fibrosis, while emerging targeted anti-fibrotic therapies have shown promise in reducing fibrotic biomarkers, although their clinical importance remains to be established. Further research is needed to clarify the relationship between cardiac fibrosis and clinical outcomes, which will be essential for the development and implementation of novel anti-fibrotic interventions in targeted patient populations.
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Parvathaneni et al. (2026) conducted a review in Cardiac fibrosis. Targeted anti-fibrotic and antihypertensive therapies was evaluated. Targeted anti-fibrotic therapies show promise in reducing fibrotic biomarkers in human cardiac fibrosis, though their clinical importance and impact on outcomes remain to be established.
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