ArticleHeliyon2024
LncRNA Zfas1 boosts cell apoptosis and autophagy in myocardial injury induced by hypoxia via miR-383-5p/ATG10 axis.
Article in Heliyon, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- Cardiovascular diseases in the elderly: possibilities for modulating autophagy using non-coding RNAs.Frontiers in cell and developmental biology · 2025Review
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Authors and funding
5 authors.
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No grant is acknowledged in the PubMed record.
Abstract
Background: Myocardial injury has been regarded as a major cause of several heart diseases. Long non-coding RNA (lncRNA) has emerged as a key regulator in a wide array of diseases. Aim of the study: This study aims to explore the role of Zfas1 in myocardial injury. Methods: 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay was adopted to evaluate the proliferative capability of H9c2 cells. Terminal deoxynucleotidyltransferase dUTP nick end labeling (TUNEL) and flow cytometry assays were employed to measure cell apoptosis. The expression of proteins related to apoptosis and autophagy was examined by Western blot. Immunofluorescence (IF) assay was performed to monitor the process of autophagy. Real-time reverse-transcription polymerase chain reaction (RT-qPCR) was employed to determine the expressions of autophagy-related gene 10 (ATG10), miR-383-5p and Zfas1. The interacting relationship between miR-383-5p and ATG10 (or Zfas1) was assessed by luciferase reporter and RNA-binding protein immunoprecipitation (RIP) assays. Results: The treatment of hypoxia hindered cell proliferation but accelerated cell apoptosis and autophagy. ATG10 exhibited higher mRNA and protein expression in H9c2 cells induced by hypoxia. MiR-383-5p was revealed to be the upstream gene of ATG10 and could interact with ATG10. Zfas1 was validated to sponge miR-383-5p and positively regulated ATG10 expression. Zfas1 knockdown-mediated cellular proliferation, apoptosis and autophagy phenotypes were counteracted by ATG10 abundance. Conclusions: LncRNA Zfas1 boosts cell apoptosis and autophagy in myocardial injury induced by hypoxia via miR-383-5p/ATG10 axis, indicating that Zfas1 may be utilized as a therapeutic target for myocardial injury.
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