ArticleCardiovascular research2017
Serelaxin treatment promotes adaptive hypertrophy but does not prevent heart failure in experimental peripartum cardiomyopathy.
Article in Cardiovascular research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 2 of them syntheses that pooled it.
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Who cites it
15 citing papers in PubMed, 2 syntheses or guidelines pooled it, 30 citations in OpenAlex.
- Prolactin Inhibition in Peripartum Cardiomyopathy: Systematic Review and Meta-analysis.Current problems in cardiology · 2023Pooled it
- Systematic review and meta-analysis of prolactin and iron deficiency in peripartum cardiomyopathy.Open heart · 2020Pooled it
- Ufmylation Suppresses Unfolded Protein Response to Prevent Peripartum Cardiomyopathy.JACC. Basic to translational science · 2025Article
- Aims and Rationale of a National Registry Integrating Clinical, Echocardiographic, and Multi-Omics Profiling to Promote Precision Medicine in Peripartum Cardiomyopathy.Biomedicines · 2025Article
- Computational model captures cardiac growth in hypertensive pregnancies and in the postpartum period.American journal of physiology. Heart and circulatory physiology · 2024Article
- Significance of plasma relaxin-2 levels in patients with primary hypertension and type 2 diabetes mellitus.Wiener medizinische Wochenschrift (1946) · 2024Article
- Animal Models of Cardiovascular Complications of Pregnancy.Circulation research · 2022Review
- Review
- Anthracycline-free tumor elimination in mice leads to functional and molecular cardiac recovery from cancer-induced alterations in contrast to long-lasting doxorubicin treatment effects.Basic research in cardiology · 2021Article
- Energy metabolism disorders and potential therapeutic drugs in heart failure.Acta pharmaceutica Sinica. B · 2021Review
- NF-kB signaling in cardiomyocytes is inhibited by sevoflurane and promoted by propofol.FEBS open bio · 2020Article
- Peripartum Cardiomyopathy: an Update.Current heart failure reports · 2018Review
- Transcriptional up-regulation of relaxin-3 by Nur77 attenuates β-adrenergic agonist-induced apoptosis in cardiomyocytes.The Journal of biological chemistry · 2018Article
- Relaxin activates AMPK-AKT signaling and increases glucose uptake by cultured cardiomyocytes.Endocrine · 2018Article
- The Role of Genetics in Peripartum Cardiomyopathy.Journal of cardiovascular translational research · 2017Review
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimsPeripartum cardiomyopathy (PPCM) is a systolic left ventricular dysfunction developing in the peripartum phase in previously healthy women. Relaxin-2 is a pregnancy hormone with potential beneficial effects in heart failure patients. We evaluated Relaxin-2 as a potential diagnostic marker and/or a therapeutic agent in PPCM. METHODS AND
resultsIn healthy peripartum women, serum Relaxin-2 levels (measured by ELISA in the second half of pregnancy) were elevated showing a decreasing trend in the first postpartum week and returned to non-pregnant levels thereafter. In PPCM patients diagnosed in the first postpartum week, serum Relaxin-2 levels were lower compared to healthy postpartum stage-matched controls. In PPCM patients diagnosed later (0.5-10 months postpartum) Relaxin-2 levels were in the range of non-pregnant controls and not different from healthy postpartum stage-matched controls. In mice, serum Relaxin-1 (functional equivalent of human Relaxin-2) was increased late in pregnancy and rapidly cleared in the first postpartum week. In mice with PPCM due to a cardiomyocyte-specific knockout of STAT3 (CKO) neither low nor high dose of recombinant Relaxin-2 (serelaxin, sRlx-LD: 30 µg/kg/day; sRlx-HD: 300 µg/kg/day) affected cardiac fibrosis, inflammation and heart failure but sRlx-HD increased capillary/cardiomyocyte ratio. sRlx-HD significantly increased heart/body weight ratio and cardiomyocyte cross-sectional area in postpartum CKO and wild-type mice without changing the foetal gene expression program (ANP or β-MHC). sRlx-HD augmented plasma Prolactin levels in both genotypes, which induced cardiac activation of STAT5. In vitro analyses showed that Prolactin induces cardiomyocyte hypertrophy via activation of STAT5.
conclusionAlthough Relaxin-2 levels seemed lower in PPCM patients diagnosed early postpartum, we observed a high pregnancy-related variance of serum Relaxin-2 levels peripartum making it unsuitable as a biomarker for this condition. Supplementation with sRlx may contribute to angiogenesis and compensatory hypertrophy in the diseased heart, but the effects are not sufficient to prevent heart failure in an experimental PPCM model.
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