Article3 Biotech2019
Aberrant expression of TNRC6a and miR-21 during myocardial infarction.
Article in 3 Biotech, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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
5 citing papers in PubMed, 8 citations in OpenAlex.
- The European BestAgeing Study on microRNA candidates reveals distinct signatures with diagnostic and prognostic potential in cardiovascular disease.BMC medicine · 2025Article
- Bioinformatics Analysis of Next Generation Sequencing Data Identifies Molecular Biomarkers Associated With Type 2 Diabetes Mellitus.Clinical medicine insights. Endocrinology and diabetes · 2023Article
- Argon inhibits reactive oxygen species oxidative stress via the miR-21-mediated PDCD4/PTEN pathway to prevent myocardial ischemia/reperfusion injury.Bioengineered · 2021Article
- MicroRNAs in Hypertrophic, Arrhythmogenic and Dilated Cardiomyopathy.Diagnostics (Basel, Switzerland) · 2021Review
- Downregulation of Long Noncoding RNA LINC00261 Attenuates Myocardial Infarction through the miR-522-3p/Trinucleotide Repeat-Containing Gene 6a (TNRC6A) Axis.Cardiovascular therapeutics · 2021Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In the present study, aberrant expression of trinucleotide repeat-containing gene 6a (TNRC6a) and miR-21 was noted and documented in rat myocardial infarction. Briefly, Sprague-Dawley rat model was used for the development of myocardial infarction. Experiments such as histological analysis were carried out to confirm the histopathology of the myocardial infarction. The expression profile of TNRC6a and miR-21 was identified by using quantitative real-time PCR. In addition, immunoblotting was performed to validate the expression profile of TNRC6a and phosphatase and tensin homolog (PTEN). The histological analysis confirmed the progress of myocardial infarction in rat model. As the disease progresses, the protein TNRC6a expresses abnormally which in turn up-regulates the miR-21 after 3rd and 5th week of infarction. Interestingly, miR-21 binds with its specific target genes PTEN and thereby degrades the target mRNA; as a result, its expression was down-regulated progressively and paved the development of myocardial infarction. The present study concludes that the aberrant expression of TNRC6a and miR-21 was documented during myocardial infarction. These findings play an important role in the diagnosis as well as pave a way for the development of drug targets for treating myocardial infarction.
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