ArticleThe Journal of cell biology2006
Follistatin induction by nitric oxide through cyclic GMP: a tightly regulated signaling pathway that controls myoblast fusion.
Article in The Journal of cell biology, 2006. 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 It has been retracted, and should not be counted.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 42 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
42 citing papers in PubMed, 104 citations in OpenAlex.
- Enhancing health span: muscle stem cells and hormesis.Biogerontology · 2022Review
- Key concepts in muscle regeneration: muscle "cellular ecology" integrates a gestalt of cellular cross-talk, motility, and activity to remodel structure and restore function.European journal of applied physiology · 2022Review
- Fusion and beyond: Satellite cell contributions to loading-induced skeletal muscle adaptation.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021Review
- Article
- Location, Location, Location: Signals in Muscle Specification.Journal of developmental biology · 2018Review
- TGF-β Family Signaling in Mesenchymal Differentiation.Cold Spring Harbor perspectives in biology · 2018Review
- SIRT1 may play a crucial role in overload-induced hypertrophy of skeletal muscle.The Journal of physiology · 2017Article
- Skeletal muscle tissue engineering: methods to form skeletal myotubes and their applications.Tissue engineering. Part B, Reviews · 2014Review
- Next-generation sequencing analysis of miRNA expression in control and FSHD myogenesis.PloS one · 2014Article
- Oxygen consumption and usage during physical exercise: the balance between oxidative stress and ROS-dependent adaptive signaling.Antioxidants & redox signaling · 2013Review
- Requirement of inducible nitric oxide synthase for skeletal muscle regeneration after acute damage.Journal of immunology (Baltimore, Md. : 1950) · 2013Article
- Mammalian target of rapamycin (mTOR) signaling network in skeletal myogenesis.The Journal of biological chemistry · 2012Review
- Nitric oxide in myogenesis and therapeutic muscle repair.Molecular neurobiology · 2012Review
- Liver cell line derived conditioned medium enhances myofibril organization of primary rat cardiomyocytes.Molecules and cells · 2012Article
- Emerging drugs for Duchenne muscular dystrophy.Expert opinion on emerging drugs · 2012Review
- Marking the tempo for myogenesis: Pax7 and the regulation of muscle stem cell fate decisions.Journal of cellular and molecular medicine · 2012Review
- Pre-clinical drug tests in the mdx mouse as a model of dystrophinopathies: an overview.Acta myologica : myopathies and cardiomyopathies : official journal of the Mediterranean Society of Myology · 2012Review
- Nitric oxide synthase inhibition prevents activity-induced calcineurin-NFATc1 signalling and fast-to-slow skeletal muscle fibre type conversions.The Journal of physiology · 2012Article
- Nitric oxide sustains long-term skeletal muscle regeneration by regulating fate of satellite cells via signaling pathways requiring Vangl2 and cyclic GMP.Stem cells (Dayton, Ohio) · 2012Article
- Necdin enhances myoblasts survival by facilitating the degradation of the mediator of apoptosis CCAR1/CARP1.PloS one · 2012Article
Corrections and comments
- Retraction · 2013-02-04Duplication of/in Image · Investigation by Journal/Publisher · Manipulation of Images · Unreliable Results and/or Conclusions ·
- Retracted
Authors and funding
9 authors at 5 institutions in 2 countries.
Funding
Abstract
The mechanism of skeletal myoblast fusion is not well understood. We show that endogenous nitric oxide (NO) generation is required for myoblast fusion both in embryonic myoblasts and in satellite cells. The effect of NO is concentration and time dependent, being evident only at the onset of differentiation, and direct on the fusion process itself. The action of NO is mediated through a tightly regulated activation of guanylate cyclase and generation of cyclic guanosine monophosphate (cGMP), so much so that deregulation of cGMP signaling leads to a fusion-induced hypertrophy of satellite-derived myotubes and embryonic muscles, and to the acquisition of fusion competence by myogenic precursors in the presomitic mesoderm. NO and cGMP induce expression of follistatin, and this secreted protein mediates their action in myogenesis. These results establish a hitherto unappreciated role of NO and cGMP in regulating myoblast fusion and elucidate their mechanism of action, providing a direct link with follistatin, which is a key player in myogenesis.
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.