ArticleAmerican journal of physiology. Heart and circulatory physiology2009
Silencing the myotrophin gene by RNA interference leads to the regression of cardiac hypertrophy.
Article in American journal of physiology. Heart and circulatory physiology, 2009. 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 It has been retracted, and should not be counted.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 8 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.
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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
8 citing papers in PubMed, 15 citations in OpenAlex.
- Non-coding RNAs in cardiovascular diseases: diagnostic and therapeutic perspectives.European heart journal · 2018Review
- MicroRNA-regulated viral vectors for gene therapy.World journal of experimental medicine · 2016Review
- CPI motif interaction is necessary for capping protein function in cells.Nature communications · 2015Article
- Capping protein regulators fine-tune actin assembly dynamics.Nature reviews. Molecular cell biology · 2014Review
- Transfer and Expression of Small Interfering RNAs in Mammalian Cells Using Lentiviral Vectors.Acta naturae · 2013Article
- In vivo, cardiac-specific knockdown of a target protein, malic enzyme-1, in rat via adenoviral delivery of DNA for non-native miRNA.Current gene therapy · 2012Article
- Lentiviral vectors and cardiovascular diseases: a genetic tool for manipulating cardiomyocyte differentiation and function.Gene therapy · 2012Review
- Molecular characterization, expression patterns and subcellular localization of Myotrophin (MTPN) gene in porcine skeletal muscle.Molecular biology reports · 2012Article
Corrections and comments
- Retraction · 2021-02-17Falsification/Fabrication of Image · Investigation by Company/Institution · Manipulation of Images · Objections by Author(s) ·
- Retracted
Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Myotrophin-induced activation of NF-kappaB has been shown to be associated with cardiac hypertrophy (CH) that progresses to heart failure (HF). In the present study, we examined the cause-and-effect relationship between myotrophin and NF-kappaB activation using small hairpin RNA (shRNA) against myotrophin both in vitro (using neonatal rat myocytes) and in vivo [using myotrophin transgenic (Myo-Tg) mice, which overexpress myotrophin in the heart, develop CH, and gradually progress to HF]. Among several lentiviral vectors expressing myotrophin shRNAs, L-sh-109 showed the best silencing effect at both the mRNA (155.3 +/- 5.9 vs. 32.5 +/- 5.5, P < 0.001) and protein levels associated with a significant reduction of atrial natriuretic factor (ANF) and NF-kappaB. In vivo, when L-sh-109 was delivered directly into the hearts of 10-wk-old Myo-Tg mice, we observed a significant regression of cardiac mass (8.0 vs. 5.7 mg/g, P < 0.001) and myotrophin gene expression (54.5% over untreated Myo-Tg mice, P < 0.001) associated with a reduction in ANF and NF-kappaB signaling components. Our data suggest that using RNA interference to silence the myotrophin gene prevents NF-kappaB activation, associated with an attenuation of CH. This strategy could be an excellent therapeutic means for the treatment of CH and HF.
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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.