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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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.
Hamouz et al. (Thu,) reported a other. 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.