ArticlePloS one2014
Pitx2c is reactivated in the failing myocardium and stimulates myf5 expression in cultured cardiomyocytes.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 17 citations in OpenAlex.
- Atrial cardiomyopathy: From healthy atria to atrial failure. A clinical consensus statement of the Heart Failure Association of the ESC.European journal of heart failure · 2025Article
- PITX2 induction leads to impaired cardiomyocyte function in arrhythmogenic cardiomyopathy.Stem cell reports · 2023Article
- Identification of atrial-enriched lncRNA Walras linked to cardiomyocyte cytoarchitecture and atrial fibrillation.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2022Article
- Case report: Congenital mitral and tricuspid valve insufficiency in a patient with Axenfeld-Rieger syndrome.Frontiers in cardiovascular medicine · 2022Article
- Full-Length Transcriptome Sequencing: An Insight Into the Dog Model of Heart Failure.Frontiers in cardiovascular medicine · 2021Article
- Pterostilbene Attenuates Fructose-Induced Myocardial Fibrosis by Inhibiting ROS-Driven Pitx2c/miR-15b Pathway.Oxidative medicine and cellular longevity · 2019Article
- Interplay between cardiac transcription factors and non-coding RNAs in predisposing to atrial fibrillation.Journal of molecular medicine (Berlin, Germany) · 2018Review
- Myocardial transcription factors in diastolic dysfunction: clues for model systems and disease.Heart failure reviews · 2016Review
- PITX2 Loss-of-Function Mutation Contributes to Congenital Endocardial Cushion Defect and Axenfeld-Rieger Syndrome.PloS one · 2015Article
- A MicroRNA-Transcription Factor Blueprint for Early Atrial Arrhythmogenic Remodeling.BioMed research international · 2015Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundPitx2 (paired-like homeodomain 2 transcription factor) is crucial for heart development, but its role in heart failure (HF) remains uncertain. The present study lays the groundwork implicating Pitx2 signalling in different modalities of HF. METHODOLOGY/PRINCIPAL
findingsA variety of molecular, cell-based, biochemical, and immunochemical assays were used to evaluate: (1) Pitx2c expression in the porcine model of diastolic HF (DHF) and in patients with systolic HF (SHF) due to dilated and ischemic cardiomyopathy, and (2) molecular consequences of Pitx2c expression manipulation in cardiomyocytes in vitro. In pigs, the expression of Pitx2c, physiologically downregulated in the postnatal heart, is significantly re-activated in left ventricular (LV) failing myocardium which, in turn, is associated with increased expression of a restrictive set of Pitx2 target genes. Among these, Myf5 was identified as the top upregulated gene. In vitro, forced expression of Pitx2c in cardiomyocytes, but not in skeletal myoblasts, activates Myf5 in dose-dependent manner. In addition, we demonstrate that the level of Pitx2c is upregulated in the LV-myocardium of SHF patients. CONCLUSIONS/SIGNIFICANCE: The results provide previously unrecognized evidence that Pitx2c is similarly reactivated in postnatal/adult heart at distinct HF phenotypes and suggest that Pitx2c is involved, directly or indirectly, in the regulation of Myf5 expression in cardiomyocytes.
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