ArticleBioengineered2022
Long non-coding RNA muscleblind like splicing regulator 1 antisense RNA 1 (LncRNA MBNL1-AS1) promotes the progression of acute myocardial infarction by regulating the microRNA-132-3p/SRY-related high-mobility-group box 4 (SOX4) axis.
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 It has been retracted, and should not be counted.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 7 papers.
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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
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
7 citing papers in PubMed, 10 citations in OpenAlex.
- APEX1 Knockdown Alleviates Inflammation and Fibrosis in Myocardial Infarction Through Promoting ZCCHC9 Expression and Blocking the p38 MAPK Signaling.Biochemical genetics · 2025Article
- Noncoding RNAs as Key Regulators for Cardiac Development and Cardiovascular Diseases.Journal of cardiovascular development and disease · 2023Review
- LncRNA MBNL1-AS1 Suppresses Cell Proliferation and Metastasis of Pancreatic Adenocarcinoma through Targeting Carcinogenic miR-301b-3p.Genetics research · 2023Article
- The expression profile of lung long non-coding RNAs and mRNAs in a mouse model of smoke inhalation injury.Bioengineered · 2022Article
- LncRNA MBNL1-AS1 represses gastric cancer progression via the TGF-β pathway by modulating miR-424-5p/Smad7 axis.Bioengineered · 2022Article
- Tanshinone IIA alleviates cardiac hypertrophy through m6A modification of galectin-3.Bioengineered · 2022Article
- Exosomes derived from mesenchymal stem cells ameliorate impaired glucose metabolism in myocardial Ischemia/reperfusion injury through miR-132-3p/PTEN/AKT pathway.Cell cycle (Georgetown, Tex.)Article
Corrections and comments
- Retraction · 2024-02-20Concerns/Issues about Data · Concerns/Issues about Results and/or Conclusions · Investigation by Journal/Publisher · Original Data and/or Images not Provided and/or not Available ·
- Retracted
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Long non-coding RNA muscleblind like splicing regulator 1 antisense RNA 1 (LncRNA MBNL1-AS1) exerts vital role in various physiological processes. However, its functions in acute myocardial infarction (AMI) are not elucidated. AMI model was constructed using Wistar rats and it was found that LncRNA MBNL1-AS1 was upregulated in AMI model according to the quantitative real-time polymerase chain reaction (qRT-PCR) results. The left ventricular systolic pressure (LVSP), left ventricular end diastolic pressure (LVEDP) and maximum rate of rise/fall of left ventricle pressure (±dp/dt max) were detected through hemodynamics test, which showed that knockdown of MBNL1-AS1 improved cardiac function in AMI model. Next, the myocardial infarction area was estimated by triphenyltetrazole chloride (TTC) staining, and the levels of cardiac troponin I (cTn-I) and creatine kinase-MB (CK-MB) were detected by enzyme-linked immunosorbent assay (ELISA) kit. The results revealed that silencing MBLN1-AS1 alleviated myocardial injury in AMI model. Additionally, MBNL1-AS1 knockdown inhibited apoptosis of myocardial cells and reduced the expression of apoptotic proteins. According to DIANA database and luciferase reporter assay, miR-132-3p was the direct target of MBNL1-AS1 and was negatively regulated by MBNL1-AS1. Furthermore, Targetscan database predicted that SRY-related high-mobility-group box 4 (SOX4) was the direct target of miR-132-3p and was regulated by MBNL1-AS1 through miR-132-3p. Moreover, overexpression of SOX4 partially eliminated effects of MBNL1-AS1 on myocardial cells. In conclusion, this investigation for the first time revealed that LncRNA MBNL1-AS1 was the potential target for treating AMI and expounded the underlying mechanisms of it.
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