ArticlePloS one2013
Conditional expression of TGF-β1 in skeletal muscles causes endomysial fibrosis and myofibers atrophy.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 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
26 citing papers in PubMed, 61 citations in OpenAlex.
- Multi-omic integrated networks connect DNA methylation and miRNA with skeletal muscle plasticity to chronic exercise in Type 2 diabetic obesity.Physiological genomics · 2014Trial
- Skeletal muscle‑derived extracellular vesicles in multi‑organ degenerative disease: Mechanisms and therapeutic delivery perspectives (Review).International journal of molecular medicine · 2026Review
- Resistance-exercise-induced stress intervenes in TGF-β signaling by cooperatively downregulating nuclear αB-crystallin and SMAD4 in human skeletal muscle fibers.The FEBS journal · 2026Article
- SMAD2 ubiquitination through PY motif regulates skeletal muscle mass and fibrotic degeneration.Scientific reports · 2026Article
- Regulatory role of vitamin DScientific reports · 2025Article
- Reduced myotube diameter induced by combined inhibition of transforming growth factor-β type I receptors Acvr1b and Tgfbr1 is associated with enhanced β1-syntrophin expression.Journal of cellular physiology · 2024Article
- Article
- The Adiponectin Receptor Agonist, ALY688: A Promising Therapeutic for Fibrosis in the Dystrophic Muscle.Cells · 2023Article
- Lack ofeLife · 2022Article
- Out of Control: The Role of the Ubiquitin Proteasome System in Skeletal Muscle during Inflammation.Biomolecules · 2021Review
- Maslinic Acid Attenuates Denervation-Induced Loss of Skeletal Muscle Mass and Strength.Nutrients · 2021Article
- Increased immunosuppression impairs tissue homeostasis with aging and age-related diseases.Journal of molecular medicine (Berlin, Germany) · 2021Review
- Morphological Alteration and TGF-β1 Expression in Multifidus with Lumbar Disc Herniation.Indian journal of orthopaedics · 2020Article
- Multiple Roles of Transforming Growth Factor Beta in Amyotrophic Lateral Sclerosis.International journal of molecular sciences · 2020Review
- ER stress activates immunosuppressive network: implications for aging and Alzheimer's disease.Journal of molecular medicine (Berlin, Germany) · 2020Review
- Article
- Morphometric and Molecular Muscle Remodeling after Passive Stretching in Elderly Female Rats.Clinics (Sao Paulo, Brazil) · 2020Article
- Erythropoietin Alleviates Burn-induced Muscle Wasting.International journal of medical sciences · 2020Article
- Role of Transforming Growth Factor-β in Skeletal Muscle Fibrosis: A Review.International journal of molecular sciences · 2019Review
- HMGB1/autophagy pathway mediates the atrophic effect of TGF-β1 in denervated skeletal muscle.Cell communication and signaling : CCS · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
To study the effects of transforming growth factor beta 1 (TGF-β1) on fibrosis and failure of regeneration of skeletal muscles, we generated a tet-repressible muscle-specific TGF-β1 transgenic mouse in which expression of TGF-β1 is controlled by oral doxycycline. The mice developed muscle weakness and atrophy after TGF-β1 over-expression. We defined the group of mice that showed phenotype within 2 weeks as early onset (EO) and the rest as late onset (LO), which allowed us to further examine phenotypic differences between the groups. While only mice in the EO group showed significant muscle weakness, pathological changes including endomysial fibrosis and smaller myofibers were observed in both groups at two weeks after the TGF-β1 was over-expressed. In addition, the size of the myofibers and collagen accumulation were significantly different between the two groups. The amount of latent and active TGF-β1 in the muscle and circulation were significantly higher in the EO group compared to the LO or control groups. The up-regulation of the latent TGF-β1 indicated that endogenous TGF-β1 was induced by the expression of the TGF-β1 transgene. Our studies showed that the primary effects of TGF-β1 over-expression in skeletal muscles are muscle wasting and endomysial fibrosis. In addition, the severity of the pathology is associated with the total amount of TGF-β1 and the expression of endogenous TGF-β1. The findings suggest that an auto-feedback loop of TGF-β1 may contribute to the severity of phenotypes.
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.