ArticleJournal of cellular and molecular medicine2012
Relaxin promotes growth and maturation of mouse neonatal cardiomyocytes in vitro: clues for cardiac regeneration.
Article in Journal of cellular and molecular medicine, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
16 citing papers in PubMed, 32 citations in OpenAlex.
- Relaxin-2 as a Potential Biomarker in Cardiovascular Diseases.Journal of personalized medicine · 2022Review
- Serelaxin activates eNOS, suppresses inflammation, attenuates developmental delay and improves cognitive functions of neonatal rats after germinal matrix hemorrhage.Scientific reports · 2020Article
- Genetic and epigenetic regulation of cardiomyocytes in development, regeneration and disease.Development (Cambridge, England) · 2018Review
- Relaxin activates AMPK-AKT signaling and increases glucose uptake by cultured cardiomyocytes.Endocrine · 2018Article
- Structural commonality of C1q TNF-related proteins and their potential to activate relaxin/insulin-like family peptide receptor 1 signalling pathways in cancer cells.British journal of pharmacology · 2017Review
- HYDAMTIQ, a selective PARP-1 inhibitor, improves bleomycin-induced lung fibrosis by dampening the TGF-β/SMAD signalling pathway.Journal of cellular and molecular medicine · 2017Article
- Sphingosine 1-Phosphate Receptors: Do They Have a Therapeutic Potential in Cardiac Fibrosis?Frontiers in pharmacology · 2017Review
- Relaxin-2 in Cardiometabolic Diseases: Mechanisms of Action and Future Perspectives.Frontiers in physiology · 2017Review
- Role of sphingosine kinase/S1P axis in ECM remodeling of cardiac cells elicited by relaxin.Molecular endocrinology (Baltimore, Md.) · 2015Article
- Serelaxin: a novel therapy for acute heart failure with a range of hemodynamic and non-hemodynamic actions.American journal of cardiovascular drugs : drugs, devices, and other interventions · 2014Review
- Role of protein kinase C β₂ in relaxin-mediated inhibition of cardiac fibrosis.Journal of endocrinological investigation · 2014Article
- Model systems for cardiovascular regenerative biology.Cold Spring Harbor perspectives in medicine · 2013Review
- 3D engineered cardiac tissue models of human heart disease: learning more from our mice.Trends in cardiovascular medicine · 2013Review
- Relaxin prevents cardiac fibroblast-myofibroblast transition via notch-1-mediated inhibition of TGF-β/Smad3 signaling.PloS one · 2013Article
- Trophic actions of bone marrow-derived mesenchymal stromal cells for muscle repair/regeneration.Cells · 2012Article
- Potential Application of Modified mRNA in Cardiac Regeneration.Cell transplantationReview
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The demonstration that the adult heart contains myocardial progenitor cells which can be recruited in an attempt to replace the injured myocardium has sparkled interest towards novel molecules capable of improving the differentiation of these cells. In this context, the peptide hormone relaxin (RLX), recently validated as a cardiovascular hormone, is a promising candidate. This study was designed to test the hypothesis that RLX may promote the growth and maturation of mouse neonatal immature cardiomyocytes in primary culture. The cultures were studied at 2, 12, 24 and 48 hrs after the addition of human recombinant H2 RLX (100 ng/ml), the main circulating form of the hormone, or plain medium by combining molecular biology, morphology and electrophysiology. RLX modulated cell proliferation, promoting it at 2 and 12 hrs and inhibiting it at 24 hrs; RLX also induced the expression of both cardiac-specific transcription factors (GATA-4 and Nkx2-5) and cardiac-specific structural genes (connexin 43, troponin T and HCN4 ion channel) at both the mRNA and protein level. Consistently, RLX induced the appearance of ultrastructural and electrophysiological signs of functionally competent, mature cardiomyocytes. In conclusion, this study provides novel circumstantial evidence that RLX specifically acts on immature cardiomyocytes by promoting their proliferation and maturation. This notion suggests that RLX, for which the heart is both a source and target organ, may be an endogenous regulator of cardiac morphogenesis during pre-natal life and could participate in heart regeneration and repair, both as endogenous myocardium-derived factor and exogenous cardiotropic drug, during adult life.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.