ArticleInternational journal of molecular sciences2019
β-catenin/LEF1/IGF-IIR Signaling Axis Galvanizes the Angiotensin-II- induced Cardiac Hypertrophy.
Article in International journal of molecular sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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Who cites it
6 citing papers in PubMed, 19 citations in OpenAlex.
- Goreisan attenuates cardiac hypertrophy and diastolic dysfunction in heart failure with preserved ejection fraction induced by HFD/L-NAME via regulation of ICAT-β-catenin/ERK axis.Hypertension research : official journal of the Japanese Society of Hypertension · 2025Article
- Epigenetic biomarkers predict macrovascular events in individuals with type 2 diabetes.Cell reports. Medicine · 2025Article
- Accumulated β-catenin is associated with human atrial fibrosis and atrial fibrillation.Journal of translational medicine · 2024Article
- Association of DNA methylation and transcriptome reveals epigenetic etiology of heart failure.Functional & integrative genomics · 2022Article
- β-Catenin Regulates Cardiac Energy Metabolism in Sedentary and Trained Mice.Life (Basel, Switzerland) · 2020Article
- Endogenous CCN5 Participates in Angiotensin II/TGF-βFrontiers in pharmacology · 2020Article
Corrections and comments
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Authors and funding
10 authors at 7 institutions in 2 countries.
Funding
Abstract
Cardiovascular diseases have a high prevalence worldwide and constitute the leading causes of mortality. Recently, malfunctioning of β-catenin signaling has been addressed in hypertensive heart condition. Ang-II is an important mediator of cardiovascular remodeling processes which not only regulates blood pressure but also leads to pathological cardiac changes. However, the contribution of Ang-II/β-catenin axis in hypertrophied hearts is ill-defined. Employing in vitro H9c2 cells and in vivo spontaneously hypertensive rats (SHR) cardiac tissue samples, western blot analysis, luciferase assays, nuclear-cytosolic protein extracts, and immunoprecipitation assays, we found that under hypertensive condition β-catenin gets abnormally induced that co-activated LEF1 and lead to cardiac hypertrophy changes by up-regulating the IGF-IIR signaling pathway. We identified putative LEF1 consensus binding site on IGF-IIR promoter that could be regulated by β-catenin/LEF1 which in turn modulate the expression of cardiac hypertrophy agents. This study suggested that suppression of β-catenin expression under hypertensive condition could be exploited as a clinical strategy for cardiac pathological remodeling processes.
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Registered trials
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