ArticleIn vitro cellular & developmental biology. Animal2020
DSCAM-AS1 mediates pro-hypertrophy role of GRK2 in cardiac hypertrophy aggravation via absorbing miR-188-5p.
Article in In vitro cellular & developmental biology. Animal, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
4 citing papers in PubMed, 10 citations in OpenAlex.
- Targeting lncRNA DSCAM-AS1 for disease diagnosis and therapy.Non-coding RNA research · 2026Review
- Circ_nuclear factor I X (circNfix) attenuates pressure overload-induced cardiac hypertrophy via regulating miR-145-5p/ATF3 axis.Bioengineered · 2021Article
- New Molecular and Organelle Alterations Linked to Down Syndrome Heart Disease.Frontiers in genetics · 2021Review
- Long Non-Coding RNAs in Atrial Fibrillation: Pluripotent Stem Cell-Derived Cardiomyocytes as a Model System.International journal of molecular sciences · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Sustained cardiac hypertrophy, as previously clarified, serves as a critical initiator of heart failure and therefore is acknowledged as an important factor for heart failure treatment. The broadly demonstrated function and participation of long non-coding RNAs (lncRNAs) in tumors are well accepted. However, the underlying mechanism implicating lncRNAs in cardiac hypertrophy is mostly unexplored and deserves to be specifically studied. The devised work was aimed to disclose the function of lncRNA DS cell adhesion molecule antisense RNA 1 (DSCAM-AS1) in angiotensin II (AngII)-induced cardiac hypertrophy. In this study, we discovered the upregulation of DSCAM-AS1 in cardiomyocytes treated with AngII by quantitative real-time polymerase chain reaction (qRT-PCR). Western blot and qRT-PCR suggested that DSCAM-AS1 silencing attenuated the highly expressed hypertrophic biomarkers including β-myosin heavy chain (β-MHC), brain natriuretic peptide (BNP), and atrial natriuretic peptide (ANP) at mRNA and protein levels. The expanded cell surface in the presence of AngII treatment area was also shrunk by DSCAM-AS1 silencing. Mechanical analysis manifested that DSCAM-AS1 sponged microRNA-188-5p to boost the pro-hypertrophy gene G protein-coupled receptor kinase 2 (GRK2) expression. Rescue experiments unveiled miR-188-5p and GRK2 managed to reverse the anti-hypertrophy impact of DSCAM-AS1 silencing. In summary, DSCAM-AS1 was identified as a positive modulator in cardiac hypertrophy through miR-188-5p decoying and GRK2 augmentation, giving rise to an enriched theoretical basis for finding a promising target in cardiac hypertrophy regulation.
Indexed as
Identifiers
What OpenQuestion 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 OpenQuestion graph.