ArticleCirculation research2025
A Vaccine Against Fibroblast Activation Protein Improves Murine Cardiac Fibrosis by Preventing the Accumulation of Myofibroblasts.
Article in Circulation research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed.
- Cell-Surface Signatures and Targets of Modulated Vascular Smooth Muscle Cells in Atherosclerosis: From State Identification to Precision Intervention.Journal of cardiovascular development and disease · 2026Review
- Cardiac fibrosis: mechanistic insights and translational advances.Molecular biomedicine · 2026Review
- Targeting FAPActa pharmaceutica Sinica. B · 2026Article
- CAR-T cells targeting fibroblast activation protein eliminate pathological fibroblasts and preserve cardiac function in a Duchenne Muscular Dystrophy murine model.Stem cell research & therapy · 2026Article
- mRNA medicine for cardiovascular disease.Nature cardiovascular research · 2026Review
- Engineered T cell therapy for the treatment of cardiac fibrosis during chronic phase of myocarditis.Theranostics · 2026Article
- Cancer-Associated Fibroblasts: Clinical Applications in Imaging and Therapy.Tomography (Ann Arbor, Mich.) · 2025Review
- FAP deficiency attenuates T2DM-associated HFpEF by suppressing the CaMKIIδ-Calcineurin A-NFATc2 signaling pathway.Clinical science (London, England : 1979) · 2025Article
- Review
- Targeting Cardiac Fibrosis With a Vaccine Against Fibroblast Activation Protein.Circulation research · 2025Article
- Nanomedicine for Diagnosis and Treatment of Cardiac Fibrosis.International journal of nanomedicine · 2025Review
- 4,8-Dicarboxyl-8,9-Iridoid-1-Glycoside Alleviates Cardiac Dysfunction After Myocardial Ischaemia-Reperfusion Injury by Activating the PI3K/AKT Pathway.Dose-response : a publication of International Hormesis SocietyArticle
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Authors and funding
17 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundMyofibroblasts are primary cells involved in chronic response-induced cardiac fibrosis. Fibroblast activation protein (FAP) is a relatively specific marker of activated myofibroblasts and a potential target molecule. This study aimed to clarify whether a vaccine targeting FAP could eliminate myofibroblasts in chronic cardiac stress model mice and reduce cardiac fibrosis.
methodsWe coadministered a FAP peptide vaccine with a cytosine-phosphate-guanine (CpG) K3 oligonucleotide adjuvant to male C57/BL6J mice and confirmed an elevation in the anti-FAP antibody titer. After continuous angiotensin II and phenylephrine administration for 28 days, we evaluated the degree of cardiac fibrosis and the number of myofibroblasts in cardiac tissues.
resultsWe found that cardiac fibrosis was significantly decreased in the FAP-vaccinated mice compared with the angiotensin II and phenylephrine control mice (3.45±1.11% versus 8.62±4.79%;
conclusionsOur study demonstrates the FAP vaccine can be a therapeutic tool for cardiac fibrosis.
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