New approach methodologies: drug screening platform to identify antifibrotic compounds.

Advances and Prospects of Cardiac Organoids in Drug Development

This review summarizes recent advances in 3D cardiac in vitro modeling technologies, outlines major cardiac model construction strategies and their technical characteristics, and discusses their applications in drug toxicity evaluation, high-throughput drug screening, disease modeling, and personalized medicine.

Drug repurposing in fibrosis: From molecular networks to antifibrotic therapeutics-A narrative review.

Fibrosis is a common pathological endpoint of chronic diseases affecting multiple organs and remains a major cause of morbidity and mortality worldwide. Despite advances in understanding fibrogenesis, current antifibrotic therapies primarily slow rather than reverse disease progression, underscoring the need for more e...

Targeting an atypical G protein-coupled receptor signaling pathway for cardiac fibrosis therapy.

Through high-throughput screening, this work identified CGS15943 (CGS) as the lead antifibrotic compound and validated its activity in human cardiac fibroblasts, three-dimensional engineered heart tissues, and animal models of HF.

Integrated Scaffold Redesign and iPSC-Based Screening Reveal Potent Antifibrotic Artemisinin Analogs in Systemic Sclerosis Models

Fibrotic diseases remain among the most intractable human disorders, largely due to the absence of therapies capable of directly modulating the core cellular programs that drive pathological matrix deposition and tissue remodeling. To address this unmet medical need, we report an integrated, chemistry-driven discovery...

Fibrosis: Bridging fundamental mechanisms to precision medicine via advanced therapeutics.

CAR-based immunotherapy for cardiac fibrosis: a new therapeutic frontier.

Cardiac fibrosis is a central pathological hallmark of diverse cardiovascular disorders, driving myocardial stiffening, ventricular dysfunction, and the progression of heart failure. Following cardiac injury, resident quiescent fibroblasts activate into pro‑fibrotic myofibroblasts, which overproduce extracellular matri...