ArticlePeerJ2023
Transcription factor EB (TFEB) improves ventricular remodeling after myocardial infarction by inhibiting Wnt/
Article in PeerJ, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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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.
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Who cites it
7 citing papers in PubMed, 4 citations in OpenAlex.
- [Integrating Bioinformatics and Machine Learning Algorithms to Screen Inflammatory Biomarkers for Atrial Fibrillation and Experimental Validation].Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition · 2026Article
- Hotspots Evolution and Cutting-Edge Trends: A Bibliometric Analysis of Autophagy in Myocardial Infarction Studies From 2007 to 2025.Cardiovascular therapeutics · 2026Review
- Prognostic utility of Wnt/β-catenin signaling pathway biomarkers in predicting outcomes of patients with ST-segment elevation myocardial infarction.Frontiers in cardiovascular medicine · 2026Article
- JZL-184 Alleviate Neurological Impairment through Regulation of Mitochondrial Transfer and Lipid Droplet Accumulation after Cardiac Arrest.Molecular neurobiology · 2025Article
- Wnt Signaling Inhibitors as Therapeutic Approach in Ischemic Heart Disease.Molecules (Basel, Switzerland) · 2024Review
- MCardiovascular diagnosis and therapy · 2024Article
- Article
Corrections and comments
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Authors and funding
13 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Adverse left ventricular remodeling after myocardial infarction (MI) compromises cardiac function and increases heart failure risk. Until now, comprehension of the role transcription factor EB (TFEB) plays after MI is limited. Objectives: The purpose of this study was to describe the effects of TFEB on fibroblasts differentiation and extracellular matrix expression after MI. Methods: AAV9 (adeno-associated virus) mediated up- and down-regulated TFEB expressions were generated in C57BL/6 mice two weeks before the MI modeling. Echocardiography, Masson, Sirius red staining immunofluorescence, and wheat germ agglutinin staining were performed at 3 days, and 1, 2, and 4 weeks after MI modeling. Fibroblasts collected from SD neonatal rats were transfected by adenovirus and siRNA, and cell counting kit-8 (CCK8), immunofluorescence, wound healing and Transwell assay were conducted. Myocardial fibrosis-related proteins were identified by Western blot. PNU-74654 (100 ng/mL) was used for 12 hours to inhibit Results: The up-regulation of TFEB resulted in reduced fibroblasts proliferation and its differentiation into myofibroblasts in vitro studies. A significant up-regulation of EF and down-regulation of myocyte area was shown in the AAV9-TFEB group. Meanwhile, decreased protein level of Conclusions: TFEB demonstrated potential in restraining fibrosis after MI by inhibiting the Wnt/
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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.