ReviewCurrent cardiology reports2010
Therapeutic potential of microRNAs in heart failure.
Review in Current cardiology reports, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 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
9 citing papers in PubMed, 19 citations in OpenAlex.
- How the proteome packages the genome for cardiovascular development.Proteomics · 2014Review
- Review
- miRNA-548c: a specific signature in circulating PBMCs from dilated cardiomyopathy patients.Journal of molecular and cellular cardiology · 2013Article
- Using microRNA as an alternative treatment for hyperlipidemia and cardiovascular disease: cardio-miRs in the pipeline.Journal of cardiovascular pharmacology · 2013Review
- Deep-sequencing of endothelial cells exposed to hypoxia reveals the complexity of known and novel microRNAs.RNA (New York, N.Y.) · 2012Article
- Understanding the role of miRNA in regulating NF-κB in blood cancer.American journal of cancer research · 2012Article
- Functional genomics applied to cardiovascular medicine.Circulation · 2011Review
- The influence of genetic polymorphisms and interacting drugs on initial response to warfarin in Chinese patients with heart valve replacement.European journal of clinical pharmacology · 2011Article
- Thioredoxin 1 negatively regulates angiotensin II-induced cardiac hypertrophy through upregulation of miR-98/let-7.Circulation research · 2011Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
There is an ongoing explosion of information about microRNAs (miRs) in cardiac disease. These small noncoding RNAs regulate protein expression by destabilization and translational inhibition of target mRNAs. Similar to mRNAs, miRs are regulated in cardiac hypertrophy and heart failure, but miR expression profiles appear to be more sensitive than mRNA signatures to changes in clinical status, suggesting that miR levels in myocardium or plasma could enhance clinical diagnostics. Single miRs can target dozens or hundreds of different mRNAs, complicating attempts to determine their individual physiologic effects. However, manipulating individual miRs by overexpression or gene ablation in experimental models has begun to unravel this conundrum: Single miRs tend to regulate numerous effectors within the same functional pathway, producing a coherent physiologic response via multiple parallel perturbations. miRs are attractive nodal therapeutic targets, and stable miR mimetics (agomiRs) and antagonists (antagomiRs) are being evaluated to prevent or reverse heart failure.
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.