ArticleBioengineered2022
Long non-coding RNA lincRNA-erythroid prosurvival attenuates inflammation by enhancing myosin heavy chain 6 stability through recruitment of heterogeneous nuclear ribonucleoprotein L in myocardial infarction.
Article in Bioengineered, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 4 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.
The trial behind it
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Who cites it
4 citing papers in PubMed, 5 citations in OpenAlex.
- Characterization of protein lactylation in healthy and ischemic mouse hearts.Frontiers in cardiovascular medicine · 2025Article
- The splicing factor hnRNPL demonstrates conserved myocardial regulation across species and is altered in heart failure.FEBS letters · 2024Article
- Article
- Noncoding RNAs as Key Regulators for Cardiac Development and Cardiovascular Diseases.Journal of cardiovascular development and disease · 2023Review
Corrections and comments
- Retracted
Authors and funding
4 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Myocardial infarction (MI), a prevalent cardiac disorder with high mortality, leads to severe heart injury associated with inflammation and cardiomyocyte apoptosis. Long non-coding RNAs have been widely found to participate in the progression of MI. Here, we aimed to explore the impact of lincRNA-erythroid prosurvival (EPS) on MI-induced inflammation and cardiomyocyte apoptosis. Significantly, lincRNA-EPS was lowly expressed in MI mice and in oxygen and glucose deprivation (OGD)-treated HL-1 cells. Echocardiography analysis revealed that lincRNA-EPS overexpression increased left ventricular ejection fraction and left ventricular fraction shortening, and decreased left ventricular internal diameter at end systole and left ventricular internal diameter at end diastole in a mouse model. In our study, the expression levels of interleukin-6, tumor necrosis factor-alpha, interleukin-1β, and interleukin-18 were upregulated in the MI mice and OGD-treated HL-1 cells, while lincRNA-EPS overexpression reversed these phenotypes. Meanwhile, lincRNA-EPS reduced MI-induced cardiomyocyte apoptosis
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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.