ArticleScientific reports2017
Serelaxin treatment reverses vascular dysfunction and left ventricular hypertrophy in a mouse model of Type 1 diabetes.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 1 of them a synthesis that pooled it.
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Who cites it
30 citing papers in PubMed, 1 synthesis or guideline pooled it, 51 citations in OpenAlex.
- The association between the gut microbiota metabolite trimethylamine N-oxide and heart failure.Frontiers in microbiology · 2024Pooled it
- Vascular effects of serelaxin in patients with stable coronary artery disease: a randomized placebo-controlled trial.Cardiovascular research · 2021Trial
- Article
- Current Therapeutic Landscape for Metabolic Dysfunction-Associated Steatohepatitis.International journal of molecular sciences · 2025Review
- Significance of plasma relaxin-2 levels in patients with primary hypertension and type 2 diabetes mellitus.Wiener medizinische Wochenschrift (1946) · 2024Article
- Time-dependent specific molecular signatures of inflammation and remodelling are associated with trimethylamine-N-oxide (TMAO)-induced endothelial cell dysfunction.Scientific reports · 2023Article
- Current challenges in the treatment of cardiac fibrosis: Recent insights into the sex-specific differences of glucose-lowering therapies on the diabetic heart: IUPHAR Review 33.British journal of pharmacology · 2023Review
- Iron accumulation and lipid peroxidation: implication of ferroptosis in diabetic cardiomyopathy.Diabetology & metabolic syndrome · 2023Review
- Epidermal growth factor receptor inhibition prevents vascular calcifying extracellular vesicle biogenesis.American journal of physiology. Heart and circulatory physiology · 2023Article
- Gut-Derived Metabolite, Trimethylamine-N-oxide (TMAO) in Cardio-Metabolic Diseases: Detection, Mechanism, and Potential Therapeutics.Pharmaceuticals (Basel, Switzerland) · 2023Review
- 3D printability and biochemical analysis of revalorized orange peel waste.International journal of bioprinting · 2023Article
- Relaxin Inhibits the Cardiac Myofibroblast NLRP3 Inflammasome as Part of Its Anti-Fibrotic Actions via the Angiotensin Type 2 and ATP (P2X7) Receptors.International journal of molecular sciences · 2022Article
- Pressurized Hot Water Extraction of Okra Seeds Reveals Antioxidant, Antidiabetic and Vasoprotective Activities.Plants (Basel, Switzerland) · 2021Article
- Anti-apoptotic and Matrix Remodeling Actions of a Small Molecule Agonist of the Human Relaxin Receptor, ML290 in Mice With Unilateral Ureteral Obstruction.Frontiers in physiology · 2021Article
- Antioxidant and Cytoprotective Effect of Quinoa (Antioxidants (Basel, Switzerland) · 2020Article
- Basic Mechanisms of Diabetic Heart Disease.Circulation research · 2020Review
- Annexin-A1 deficiency exacerbates pathological remodelling of the mesenteric vasculature in insulin-resistant, but not insulin-deficient, mice.British journal of pharmacology · 2020Article
- Speckle-tracking echocardiography combined with imaging mass spectrometry assesses region-dependent alterations.Scientific reports · 2020Article
- The Novel Small-molecule Annexin-A1 Mimetic, Compound 17b, Elicits Vasoprotective Actions in Streptozotocin-induced Diabetic Mice.International journal of molecular sciences · 2020Article
- Relaxin reduces endothelium-derived vasoconstriction in hypertension: Revealing new therapeutic insights.British journal of pharmacology · 2020Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Serelaxin prevents endothelial dysfunction in the mouse aorta ex vivo and inhibits apoptosis in cardiomyocytes under acute hyperglycaemia. Less is known about the effects of serelaxin in an in vivo mouse model of diabetes. Therefore, we tested the hypothesis in streptozotocin (STZ)-treated mice that serelaxin is able to reverse diabetes-induced vascular dysfunction and cardiac remodelling. Mice were divided into citrate buffer + placebo, STZ + placebo and STZ + serelaxin (0.5 mg/kg/d, 2 weeks) groups. After 12 weeks of diabetes, sensitivity to the endothelium-dependent agonist acetylcholine (ACh) was reduced in the mesenteric artery. This was accompanied by an enhanced vasoconstrictor prostanoid contribution and a decrease in endothelium-derived hyperpolarisation (EDH)-mediated relaxation. Serelaxin restored endothelial function by increasing nitric oxide (NO)-mediated relaxation but not EDH. It also normalised the contribution of vasoconstrictor prostanoids to endothelial dysfunction and suppressed diabetes-induced hyper-responsiveness of the mesenteric artery to angiotensin II. Similarly, diabetes reduced ACh-evoked NO-mediated relaxation in the aorta which was reversed by serelaxin. In the left ventricle, diabetes promoted apoptosis, hypertrophy and fibrosis; serelaxin treatment reversed this ventricular apoptosis and hypertrophy, but had no effect on fibrosis. In summary, serelaxin reversed diabetes-induced endothelial dysfunction by enhancing NO-mediated relaxation in the mouse vasculature and attenuating left ventricular hypertrophy and apoptosis.
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