ArticleJournal of endocrinological investigation2014
Role of protein kinase C β₂ in relaxin-mediated inhibition of cardiac fibrosis.
Article in Journal of endocrinological investigation, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
4 citing papers in PubMed, 7 citations in OpenAlex.
- Anti-fibrotic actions of relaxin.British journal of pharmacology · 2017Review
- Serelaxin treatment reverses vascular dysfunction and left ventricular hypertrophy in a mouse model of Type 1 diabetes.Scientific reports · 2017Article
- Relaxin-2 in Cardiometabolic Diseases: Mechanisms of Action and Future Perspectives.Frontiers in physiology · 2017Review
- Advanced Glycation End Products Impair Voltage-Gated K+ Channels-Mediated Coronary Vasodilation in Diabetic Rats.PloS one · 2015Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionRelaxin is a pleiotropic hormone owing endogenous antifibrosis effect on numerous organs. We demonstrated relaxin's inhibitive effect on cardiac fibrosis previously.
objectiveThe aim of this study was to investigate the role of protein kinase C (PKC) β2 in relaxin's action under high glucose conditions. METHODS AND
resultsCardiac fibroblasts (CFs) were isolated, exposed to high glucose and incubated with recombinant human relaxin (rhRLX). Western blot analysis revealed a relaxin-mediated decrease in total expression and translocation of PKCβ2, showing downregulation of PKCβ2 is involved in relaxin's action. Blocking PKCβ2 pathway with ruboxistaurin accelerated rhRLX-mediated inhibition in both proliferation of CFs and deposition of collagen.
conclusionIn conclusion, relaxin can inhibit high glucose-associated cardiac fibrosis partly through PKCβ2 pathway. Further work should be done to fully understand intracellular mechanisms of relaxin's action to accelerate its clinical use.
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