ArticleBiomaterials research2025
Myofibroblast-Targeting Extracellular Vesicles: A Promising Platform for Cardiac Fibrosis Drug Delivery.
Article in Biomaterials research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
6 citing papers in PubMed.
- Artificial intelligence virtual extracellular vesicles (AIVEVs).Bioactive materials · 2026Review
- Rational design of FAP-targeted sEVs delivered by microneedles for precision treatment of hypertrophic scars via ferroptosis in hypertrophic scar fibroblasts.Materials today. Bio · 2026Article
- Extracellular vesicles in the heart: mediators of intercellular communication in health and disease in vitro.Cell communication and signaling : CCS · 2026Review
- Nanoparticle-Based Therapeutic Strategies for Pathological Cardiac Hypertrophy: Preclinical Advances, Translational Challenges, and Future Perspectives.International journal of nanomedicine · 2026Review
- In Vivo Targeted Reprogramming of Cardiac Fibroblasts for Heart Regeneration: Advances and Therapeutic Potential.Bioengineering (Basel, Switzerland) · 2025Review
- Nanomedicine for Diagnosis and Treatment of Cardiac Fibrosis.International journal of nanomedicine · 2025Review
Corrections and comments
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Authors and funding
14 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Current pharmacological treatments for cardiac fibrosis are often limited by their efficacy and specificity, leading to marked side effects. Fibroblast activation protein (FAP) is specifically expressed on activated myofibroblasts (myoFbs) but not on resting cardiac fibroblasts, making it a promising target for cardiac fibrosis therapy. In this study, we engineered extracellular vesicles (EVs) conjugated with an anti-FAP single-chain variable fragment, termed αFAP-EVs, which specifically target myoFbs. Our results demonstrated that αFAP-EVs successfully targeted activated myoFbs in vitro and localized to fibrotic regions in isoproterenol-induced mouse hearts in vivo. To further enhance delivery efficiency, αFAP-EVs were combined with clodronate-loaded liposomes (αFAP-EL@CLD) to reduce liver accumulation and improve cardiac fibrotic site targeting. αFAP-EL@CLD loaded with cholesterol-methylated- and phosphorothioate-modified miR-29b (Agomir-29b) or the transforming growth factor beta 1 receptor inhibitor GW788388 significantly inhibited myoFb activation and reduced fibrosis in isoproterenol-induced mouse models. Importantly, these drug-loaded αFAP-EL@CLD vesicles exhibited high therapeutic efficacy with minimal systemic toxicity, attributed to their stability and targeted delivery capabilities. These findings suggest that αFAP-EL@CLD vesicles are promising candidates for cardiac fibrosis therapy, offering a foundation for future clinical applications.
Identifiers
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.