ReviewThe FEBS journal2013
Modifying muscular dystrophy through transforming growth factor-β.
Review in The FEBS journal, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers, 1 of them a synthesis that pooled it.
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
46 citing papers in PubMed, 1 synthesis or guideline pooled it, 70 citations in OpenAlex.
- Inflammatory Profile of Older Adults in Response to Physical Activity and Diet Supplementation: A Systematic Review.International journal of environmental research and public health · 2023Pooled it
- Targeting TGF-β to Attenuate Ischemia-Reperfusion Associated Muscle Fibrosis and Enhance Regeneration: A Preclinical Study.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- Article
- Tendon, Ligament, and Muscle Injury, Osteotendinous, Myotendinous, and Muscle-to-Bone Junction Therapy Perspectives with Growth Factors and Stable Gastric Pentadecapeptide BPC 157-A Review.Pharmaceuticals (Basel, Switzerland) · 2026Review
- The Transforming Growth Factor β Genes and Susceptibility to Musculoskeletal Injuries in a Physically Active Caucasian Cohort.Journal of clinical medicine · 2026Article
- Genetic Susceptibility to Sport-Related Muscle Injuries: Insights from the Literature and Novel Gene Candidates.International journal of molecular sciences · 2025Review
- Elevated Levels of Active GSK3β in the Blood of Patients with Myotonic Dystrophy Type 1 Correlate with Muscle Weakness.International journal of molecular sciences · 2025Article
- Collagen type VI regulates TGF-β bioavailability in skeletal muscle in mice.The Journal of clinical investigation · 2025Article
- Extracellular matrix in skeletal muscle injury and atrophy: mechanisms and therapeutic implications.Journal of orthopaedic translation · 2025Review
- Regenerative inflammation: When immune cells help to re-build tissues.The FEBS journal · 2024Review
- Beneficial immune-modulatory effects of the N-163 strain ofIBRO neuroscience reports · 2023Article
- Myofiber directs macrophages IL-10-Vav1-Rac1 efferocytosis pathway in inflamed muscle following CTX myoinjury by activating the intrinsic TGF-β signaling.Cell communication and signaling : CCS · 2023Article
- Arthritis and Duchenne muscular dystrophy: the role of chondroitin sulfate and its associated proteoglycans in disease pathology and as a diagnostic marker.American journal of physiology. Cell physiology · 2023Review
- Pharmacological inhibition of HDAC6 improves muscle phenotypes in dystrophin-deficient mice by downregulating TGF-β via Smad3 acetylation.Nature communications · 2022Article
- Management of arthrofibrosis in neuromuscular disorders: a review.BMC musculoskeletal disorders · 2022Review
- Loss of α-actinin-3 confers protection from eccentric contraction damage in fast-twitch EDL muscles from aged mdx dystrophic mice by reducing pathological fibre branching.Human molecular genetics · 2022Article
- Role of Cardiac Fibroblasts in Cardiac Injury and Repair.Current cardiology reports · 2022Review
- Systemically Administered Homing Peptide Targets Dystrophic Lesions and Delivers Transforming Growth Factor-β (TGFβ) Inhibitor to Attenuate Murine Muscular Dystrophy Pathology.Pharmaceutics · 2021Article
- Optogenetic modeling of human neuromuscular circuits in Duchenne muscular dystrophy with CRISPR and pharmacological corrections.Science advances · 2021Article
- Anti-latent TGFβ binding protein 4 antibody improves muscle function and reduces muscle fibrosis in muscular dystrophy.Science translational medicine · 2021Article
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
Muscular dystrophy arises from ongoing muscle degeneration and insufficient regeneration. This imbalance leads to loss of muscle, with replacement by scar or fibrotic tissue, resulting in muscle weakness and, eventually, loss of muscle function. Human muscular dystrophy is characterized by a wide range of disease severity, even when the same genetic mutation is present. This variability implies that other factors, both genetic and environmental, modify the disease outcome. There has been an ongoing effort to define the genetic and molecular bases that influence muscular dystrophy onset and progression. Modifier genes for muscle disease have been identified through both candidate gene approaches and genome-wide surveys. Multiple lines of experimental evidence have now converged on the transforming growth factor-β (TGF-β) pathway as a modifier for muscular dystrophy. TGF-β signaling is upregulated in dystrophic muscle as a result of a destabilized plasma membrane and/or an altered extracellular matrix. Given the important biological role of the TGF-β pathway, and its role beyond muscle homeostasis, we review modifier genes that alter the TGF-β pathway and approaches to modulate TGF-β activity to ameliorate muscle disease.
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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.