ArticlePloS one2015
Regulation of Connective Tissue Growth Factor and Cardiac Fibrosis by an SRF/MicroRNA-133a Axis.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 48 citations in OpenAlex.
- Small Extracellular Vesicles in Cardioprotection, Cardiac Repair, and Regeneration: Cargo Mechanisms, Producer Cell Sources, and Translational Development.Biomedicines · 2026Review
- Impact ofJournal of cardiovascular development and disease · 2026Review
- Therapeutic potential of miR-133a-transfected bone marrow mesenchymal stem cell transplantation in improving cardiac function post-myocardial infarction.Journal of cardiothoracic surgery · 2025Article
- Whole-genome resequencing reveals the genetic diversity, population structure and selection signatures in Chinese indigenous Kele pigs.Frontiers in veterinary science · 2025Article
- MicroRNAs regulating signaling pathways in cardiac fibrosis: potential role of the exercise training.American journal of physiology. Heart and circulatory physiology · 2024Review
- A defective mechanosensing pathway affects fibroblast-to-myofibroblast transition in the old male mouse heart.iScience · 2023Article
- Retinoic acid receptor β modulates mechanosensing and invasion in pancreatic cancer cells via myosin light chain 2.Oncogenesis · 2023Article
- Metabolic regulation of the proteasome under hypoxia by Poldip2 controls fibrotic signaling in vascular smooth muscle cells.Free radical biology & medicine · 2023Article
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- Pyrrolidine Dithiocarbamate Might Mitigate Radiation-Induced Heart Damage at an Early Stage in Rats.Frontiers in pharmacology · 2022Article
- Non-ischemic dilated cardiomyopathy and cardiac fibrosis.Heart failure reviews · 2021Review
- The Impact of microRNAs in Renin-Angiotensin-System-Induced Cardiac Remodelling.International journal of molecular sciences · 2021Review
- Ccn2a is an injury-induced matricellular factor that promotes cardiac regeneration in zebrafish.Development (Cambridge, England) · 2021Article
- Multi-omic biomarker identification and validation for diagnosing warzone-related post-traumatic stress disorder.Molecular psychiatry · 2020Article
- Mechanosensing dysregulation in the fibroblast: A hallmark of the aging heart.Ageing research reviews · 2020Review
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- Dual roles of chromatin remodeling protein BRG1 in angiotensin II-induced endothelial-mesenchymal transition.Cell death & disease · 2020Article
- Clinical Significance and Potential Regulatory Mechanisms of Serum Response Factor in 1118 Cases of Thyroid Cancer Based on Gene Chip and RNA-Sequencing Data.Medical science monitor : international medical journal of experimental and clinical research · 2020Article
- Connective Tissue Growth Factor: From Molecular Understandings to Drug Discovery.Frontiers in cell and developmental biology · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Myocardial fibrosis contributes to the remodeling of heart and the loss of cardiac function leading to heart failure. SRF is a transcription factor implicated in the regulation of a large variety of genes involved in cardiac structure and function. To investigate the impact of an SRF overexpression in heart, we developed a new cardiac-specific and tamoxifen-inducible SRF overexpression mouse model by the Cre/loxP strategy. Here, we report that a high level overexpression of SRF leads to severe modifications of cardiac cytoarchitecture affecting the balance between cardiomyocytes and cardiac fibroblasts and also a profound alteration of cardiac gene expression program. The drastic development of fibrosis was characterized by intense sirius red staining and associated with an increased expression of genes encoding extracellular matrix proteins such as fibronectin, procollagen type 1α1 and type 3α1 and especially connective tissue growth factor (CTGF). Furthermore miR-133a, one of the most predominant cardiac miRNAs, is strongly downregulated when SRF is overexpressed. By comparison a low level overexpression of SRF has minor impact on these different processes. Investigation with miR-133a, antimiR-133a and AdSRF-VP16 experiments in H9c2 cardiac cells demonstrated that: 1)-miR-133a acts as a repressor of SRF and CTGF expression; 2)-a simultaneous overexpression of SRF by AdSRF-VP16 and inhibition of miR-133a by a specific antimiR increase CTGF expression; 3)-miR-133a overexpression can block the upregulation of CTGF induced by AdSRF-VP16. Taken together, these findings reveal a key role of the SRF/CTGF/miR-133a axis in the regulation of cardiac fibrosis.
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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.