ArticleCardiovascular research2015
Pharmacological inhibition of TGFβ receptor improves Nkx2.5 cardiomyoblast-mediated regeneration.
Article in Cardiovascular research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 26 citations in OpenAlex.
- A combinatorial oligonucleotide therapy to improve dystrophin restoration and dystrophin-deficient muscle health.Molecular therapy. Nucleic acids · 2025Article
- The Role of Stem Cells in the Treatment of Cardiovascular Diseases.International journal of molecular sciences · 2024Review
- Transforming growth factor-β in myocardial disease.Nature reviews. Cardiology · 2022Review
- Berberine Suppresses Lung Metastasis of CancerFrontiers in pharmacology · 2022Article
- Inhibition of TGF-β/Smad3 Signaling Disrupts Cardiomyocyte Cell Cycle Progression and Epithelial-Mesenchymal Transition-Like Response During Ventricle Regeneration.Frontiers in cell and developmental biology · 2021Article
- Cardiac Stromal Cell Patch Integrated with Engineered Microvessels Improves Recovery from Myocardial Infarction in Rats and Pigs.ACS biomaterials science & engineering · 2020Article
- Astragaloside IV protects human cardiomyocytes from hypoxia/reoxygenation injury by regulating miR-101a.Molecular and cellular biochemistry · 2020Article
- TGF-β inhibitor therapy decreases fibrosis and stimulates cardiac improvement in a pre-clinical study of chronic Chagas' heart disease.PLoS neglected tropical diseases · 2019Article
- Platelet-Inspired Nanocells for Targeted Heart Repair After Ischemia/Reperfusion Injury.Advanced functional materials · 2019Article
- The Role of the TGF-β Superfamily in Myocardial Infarction.Frontiers in cardiovascular medicine · 2019Review
- Reactivation of the Nkx2.5 cardiac enhancer after myocardial infarction does not presage myogenesis.Cardiovascular research · 2018Article
- The TGFβ superfamily in cardiac dysfunction.Acta biochimica et biophysica Sinica · 2018Review
- Nkx2.5+ Cardiomyoblasts Contribute to Cardiomyogenesis in the Neonatal Heart.Scientific reports · 2017Article
- The role of transforming growth factor (TGF)-β in the infarcted myocardium.Journal of thoracic disease · 2017Review
- iPSC-derived cardiomyocytes reveal abnormal TGF-β signalling in left ventricular non-compaction cardiomyopathy.Nature cell biology · 2016Article
- Signalling by Transforming Growth Factor Beta Isoforms in Wound Healing and Tissue Regeneration.Journal of developmental biology · 2016Review
- Developmental origin of postnatal cardiomyogenic progenitor cells.Future science OA · 2016Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
aimsOur previous study found that A83-01, a small molecule type 1 TGFβ receptor inhibitor, could induce proliferation of postnatal Nkx2.5(+) cardiomyoblasts in vitro and enhance their cardiomyogenic differentiation. The present study addresses whether A83-01 treatment in vivo could increase cardiomyogenesis and improve cardiac function after myocardial infarction through an Nkx2.5(+) cardiomyoblast-dependent process. METHODS AND
resultsTo determine the effect of A83-01 on the number of Nkx2.5(+) cardiomyoblasts in the heart after myocardial injury, we treated transgenic Nkx2.5 enhancer-GFP reporter mice for 7 days with either A83-01 or DMSO and measured the number of GFP(+) cardiomyoblasts in the heart at 1 week after injury by flow cytometry. To determine the degree of new cardiomyocyte formation after myocardial injury and the effect of A83-01 in this process, we employed inducible Nkx2.5 enhancer-Cre transgenic mice to lineage label postnatal Nkx2.5(+) cardiomyoblasts and their differentiated progenies after myocardial injury. We also examined the cardiac function of each animal by intracardiac haemodynamic measurements. We found that A83-01 treatment significantly increased the number of Nkx2.5(+) cardiomyoblasts at baseline and after myocardial injury, resulting in an increase in newly formed cardiomyocytes. Finally, we showed that A83-01 treatment significantly improved ventricular elastance and stroke work, leading to improved contractility after injury.
conclusionPharmacological inhibition of TGFβ signalling improved cardiac function in injured mice and promoted the expansion and cardiomyogenic differentiation of Nkx2.5(+) cardiomyoblasts. Direct modulation of resident cardiomyoblasts in vivo may be a promising strategy to enhance therapeutic cardiac regeneration.
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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.