ArticleACS pharmacology & translational science2025
Relaxin-2 Exhibits a Beneficial Role in Energy Metabolism to Alleviate Atrial Fibrillation Susceptibility.
Article in ACS pharmacology & translational science, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Relaxin-2: Shaping the Proteomic Landscape of Skeletal Muscle Physiology, Glucose Trafficking, and Mitochondrial Function in Rat.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- Observational
- Long-acting relaxin analogues: a novel tool in cardiology.Frontiers in pharmacology · 2025Review
Corrections and comments
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Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Atrial fibrillation (AF) is the most common cardiac arrhythmia, with energy metabolic disorder leading to severe clinical courses. Relaxin-2 (RLX), a peptide hormone, has been identified to activate crucial enzymes involved in cellular energy metabolism. However, whether relaxin-2 can improve the energy metabolism of atrial myocytes to inhibit AF pathogenesis remains unknown. Male New Zealand rabbits were randomly separated into sham, right atrial tachypacing (RAP), and RAP with a human recombinant relaxin-2 treatment (0.5 mg/kg) group for 2 weeks, and programmed intracardiac stimulation was performed to assess AF susceptibility. Ultrahigh-performance liquid chromatography (UHPLC) was performed to explore potential metabolic profiles in rabbit atria. Histology, transmission electron microscopy (TEM), Western blot, qRT-PCR, and Seahorse assays were used to explain the molecular mechanisms. The downregulated relaxin family peptide receptor 1 (RXFP1) protein was found in the atria of AF patients and rabbits, as well as in tachypacing HL-1 cells. RLX protected against RAP-induced AF with decreased atrial fibrosis and electrical remodeling in rabbits. UHPLC revealed that RLX improved fatty acid and glucose metabolism by activating the PPAR signaling pathway in rabbit atria. Mechanistically, RLX enhanced peroxisome proliferator-activated receptor-γ (PPARγ) expression via regulating RXFP1, which restored mitochondrial respiration and ATP production, along with reduced mitochondrial reactive oxygen species in both rabbit atria and HL-1 cells. Moreover, overexpression of
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Registered trials
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