Key result
CRISPR, CAR-T, and nanomedicine position cardiac fibrosis as a reversible target for personalized intervention.
Why the study?
Cardiac fibrosis drives myocardial stiffening and heart failure, requiring integration of mechanobiology, epigenetics, and emerging molecular tools to advance precision therapies.
Design
Review
Hypothesis-generating for reversing cardiac fibrosis in HF; extends research on CRISPR and FAP CAR-T toward trials before adoption.
Cardiac fibrosis represents a complex pathological process driven by persistent fibroblast activation, dysregulated cardiomyocyte-ECM crosstalk, and maladaptive mechanotransduction, ultimately resulting in myocardial stiffening and progressive heart failure. This review integrates insights from single-cell and spatial transcriptomics, biomechanical studies, and epigenetic profiling to illuminate the cellular heterogeneity and molecular circuits underlying fibrotic remodelling. We highlight emerging therapies including CRISPR-based gene editing, FAP-targeted CAR-T immunotherapy, nanomedicine for selective RNA delivery, and patient-derived cardiac organoids; that collectively position fibrosis as a reversible and actionable target. Finally, we discuss precision medicine strategies leveraging genomics, circulating biomarkers, artificial intelligence, and environmental risk assessment to deliver personalized anti-fibrotic interventions. By uniting mechanobiology, molecular engineering, and clinical innovation, this review charts a translational roadmap toward durable reversal of cardiac fibrosis.
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Hamouz et al. (2026) studied this question. Emerging therapies such as CRISPR gene editing, FAP-targeted CAR-T immunotherapy, and nanomedicine position cardiac fibrosis as a reversible and actionable target for personalized intervention.
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