ArticleBMC biology2026
Overexpression of Rtl1 via synonymous mutation silencing miRNA target site drives skeletal muscle hypertrophy and inflammation in mice.
Article in BMC biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- Synonymous variants in IRX4 and their association with congenital heart disease: an in-silico functional assessment.Molecular biology reports · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors.
Funding
Abstract
backgroundThe retrovirus-derived Rtl1 gene is integral to skeletal muscle development. However, the underlying mechanisms and functional roles of Rtl1 in skeletal muscle growth remain unclear.
resultsWe generated conditional overexpression of Rtl1 in mice via synonymous mutations that silence seven miRNA target sites, thereby efficiently abolishing miRNA-mediated inhibition in vivo. This conditional, specific overexpression of synonymous mutated Rtl1 (mRtl1) in the diaphragm muscles of mice foetuses resulted in aberrant embryonic diaphragm muscle development, adversely affecting both diaphragmatic and pulmonary development. This modification ultimately culminated in severe respiratory distress, leading to postnatal mortality. Subsequently, the conditional overexpression of mRtl1 in the tibialis anterior muscle of adult mice resulted in inflammation and hypertrophy. Furthermore, the overexpression of mRtl1 in cultured myotubes activated the TLR7/8-NFκB and Jak-STAT3 signalling pathways, resulting in hypertrophy and inflammation.
conclusionsThese findings suggest that the overexpression of Rtl1 may contribute to skeletal muscle hypertrophy and induce inflammation in murine models. Consequently, the precise regulation of Rtl1 expression is essential for maintaining skeletal muscle function.
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.