ArticleJournal of the American Heart Association2019
Human Relaxin-2 Fusion Protein Treatment Prevents and Reverses Isoproterenol-Induced Hypertrophy and Fibrosis in Mouse Heart.
Article in Journal of the American Heart Association, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 29 citations in OpenAlex.
- mRNA medicine for cardiovascular disease.Nature cardiovascular research · 2026Review
- Circular RNA encoding relaxin-2 as a potential therapy for liver fibrosis.Molecular therapy. Nucleic acids · 2026Article
- Gastrin ameliorates heart failure and suppresses myocardial remodeling via the JAK2/STAT3 and ERK1/2 pathways.PloS one · 2026Article
- Genomic medicine in hepatology: mechanisms and liver treatment strategies.Molecular medicine (Cambridge, Mass.) · 2025Review
- A novel long-acting relaxin-2 fusion, AZD3427, improves cardiac performance in non-human primates with cardiac dysfunction.Cardiovascular research · 2025Article
- Transient angiotensin-converting enzyme inhibition confers sex-specific protection against angiotensin II-induced cardiac remodeling.American journal of physiology. Cell physiology · 2025Article
- Long-acting relaxin analogues: a novel tool in cardiology.Frontiers in pharmacology · 2025Review
- Deletion of ASPP1 in myofibroblasts alleviates myocardial fibrosis by reducing p53 degradation.Nature communications · 2024Article
- Engineering and Characterization of a Long-Half-Life Relaxin Receptor RXFP1 Agonist.Molecular pharmaceutics · 2024Article
- Engineering a long acting, non-biased relaxin agonist using Protein-in-Protein technology.Biochemical pharmacology · 2024Article
- RNA nanotherapeutics with fibrosis overexpression and retention for MASH treatment.Nature communications · 2024Article
- Cardiomyocyte PANX1 Controls Glycolysis and Neutrophil Recruitment in Hypertrophy.Circulation research · 2024Article
- MICU3 Regulates Mitochondrial Calcium and Cardiac Hypertrophy.Circulation research · 2024Article
- Development of Novel High-Affinity Antagonists for the Relaxin Family Peptide Receptor 1.ACS pharmacology & translational science · 2023Article
- Norcantharidin induces ferroptosis via the suppression of NRF2/HO-1 signaling in ovarian cancer cells.Oncology letters · 2022Article
- TFEC contributes to cardiac hypertrophy by inhibiting AMPK/mTOR signaling.Experimental and therapeutic medicine · 2021Article
- Strategies to enhance monoclonal antibody uptake and distribution in solid tumors.Cancer biology & medicine · 2021Review
- Diverse functions of insulin-like 3 peptide.The Journal of endocrinology · 2020Review
- The relaxin family peptide receptor 1 (RXFP1): An emerging player in human health and disease.Molecular genetics & genomic medicine · 2020Review
- Human Relaxin-2 Fusion Protein Treatment Prevents and Reverses Isoproterenol-Induced Hypertrophy and Fibrosis in Mouse Heart.Journal of the American Heart Association · 2019Article
Corrections and comments
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Authors and funding
17 authors at 5 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background Heart failure is one of the leading causes of death in Western countries, and there is a need for new therapeutic approaches. Relaxin-2 is a peptide hormone that mediates pleiotropic cardiovascular effects, including antifibrotic, angiogenic, vasodilatory, antiapoptotic, and anti-inflammatory effects in vitro and in vivo. Methods and Results We developed RELAX10, a fusion protein composed of human relaxin-2 hormone and the Fc of a human antibody, to test the hypothesis that extended exposure of the relaxin-2 peptide could reduce cardiac hypertrophy and fibrosis. RELAX10 demonstrated the same specificity and similar in vitro activity as the relaxin-2 peptide. The terminal half-life of RELAX10 was 7 days in mouse and 3.75 days in rat after subcutaneous administration. We evaluated whether treatment with RELAX10 could prevent and reverse isoproterenol-induced cardiac hypertrophy and fibrosis in mice. Isoproterenol administration in mice resulted in increased cardiac hypertrophy and fibrosis compared with vehicle. Coadministration with RELAX10 significantly attenuated the cardiac hypertrophy and fibrosis compared with untreated animals. Isoproterenol administration significantly increased transforming growth factor β1 (TGF-β1)-induced fibrotic signaling, which was attenuated by RELAX10. We found that RELAX10 also significantly increased protein kinase B/endothelial NO synthase signaling and protein S-nitrosylation. In the reversal study, RELAX10-treated animals showed significantly reduced cardiac hypertrophy and collagen levels. Conclusions These findings support a potential role for RELAX10 in the treatment of heart failure.
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