ArticleAging2020
LncRNA AK045171 protects the heart from cardiac hypertrophy by regulating the SP1/MG53 signalling pathway.
Article in Aging, 2020. 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 It has been retracted, and should not be counted.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 13 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
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
13 citing papers in PubMed, 15 citations in OpenAlex.
- MG53/TRIM72: multi-organ repair protein and beyond.Frontiers in physiology · 2024Review
- Advances in the Study of MG53 in Cardiovascular Disease.International journal of general medicine · 2023Review
- The multifaceted biology of lncR-Meg3 in cardio-cerebrovascular diseases.Frontiers in genetics · 2023Review
- Article
- Long noncoding RNA H19 suppresses cardiac hypertrophy through the MicroRNA-145-3p/SMAD4 axis.Bioengineered · 2022Article
- MiR-590-5p inhibits pathological hypertrophy mediated heart failure by targeting RTN4.Journal of molecular histology · 2021Article
- Reconnoitering the Role of Long-Noncoding RNAs in Hypertrophic Cardiomyopathy: A Descriptive Review.International journal of molecular sciences · 2021Review
- The function of LncRNA-H19 in cardiac hypertrophy.Cell & bioscience · 2021Review
- Expression Profile of Long Noncoding RNAs and Circular RNAs in Mouse C3H10T1/2 Mesenchymal Stem Cells Undergoing Myogenic and Cardiomyogenic Differentiation.Stem cells international · 2021Article
- The Pivotal Role of Mitsugumin 53 in Cardiovascular Diseases.Cardiovascular toxicology · 2021Review
- Retraction Note: Inhibition of miR-296-5p protects the heart from cardiac hypertrophy by targeting CACNG6.Gene therapy · 2020Article
- The LINC01260 Functions as a Tumor Suppressor via the miR-562/CYLD/NF-κB Pathway in Non-Small Cell Lung Cancer.OncoTargets and therapy · 2020Article
- MG53 Protects against Sepsis-Induced Myocardial Dysfunction by Upregulating Peroxisome Proliferator-Activated Receptor-Oxidative medicine and cellular longevity · 2020Article
Corrections and comments
- Correction · 2020-04-03Error in Image · Updated to Retraction ·
- Retraction · 2023-02-15Euphemisms for Plagiarism · Investigation by Journal/Publisher · Plagiarism of Image · Plagiarism of Text · Upgrade/Update of Prior Notice(s) · · See also: https://pubpeer.com/publications/404B67069F893BF18880F8E86A6266
- Retracted
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hearts often undergo abnormal remodelling and hypertrophic growth in response to pathological stress. Long non-coding RNAs (LncRNAs) can change cardiac function and participate in regulation of cardiac hypertrophy. The present study aims to identify the role of AK045171 in cardiac hypertrophy and the underlying mechanism in hypertrophic cascades. Mice with cardiac hypertrophy were established through transverse aortic constriction (TAC). Cardiac hypertrophy in cardiomyocytes was induced by angiotensin II (angII). The expression of AK045171 and its target gene SP1 was examined in cardiomyocytes transfected with miRNA. The AK045171 expression level was downregulated in mice after TAC surgery. Overexpression of AK045171 attenuated cardiac hypertrophy both in vitro and in vivo. The mechanism study indicated that AK045171 binds with SP1, which promotes transcription activation of MEG3. It is suggested that overexpression of AK045171 might have clinical potential to suppress cardiac hypertrophy and heart failure.
Indexed as
Identifiers
What Socratic holds
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 Socratic graph.