ArticleMolecular endocrinology (Baltimore, Md.)2014
Myostatin augments muscle-specific ring finger protein-1 expression through an NF-kB independent mechanism in SMAD3 null muscle.
Article in Molecular endocrinology (Baltimore, Md.), 2014. 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 It has been retracted, and should not be counted.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 26 papers.
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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.
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, 46 citations in OpenAlex.
- Deletion of fibro-adipogenic progenitors-specific follistatin impairs muscle function and accelerates skeletal muscle atrophy in obese mice.Molecular medicine (Cambridge, Mass.) · 2025Article
- Contemporary insights into neuroimmune interactions across development and aging.Frontiers in neurology · 2025Review
- Upregulation of CCL5/RANTES Gene Expression in the Diaphragm of Mice with Cholestatic Liver Disease.Advances in experimental medicine and biology · 2023Article
- Inflammation: Roles in Skeletal Muscle Atrophy.Antioxidants (Basel, Switzerland) · 2022Review
- The Role of Oxidative Stress in Skeletal Muscle Myogenesis and Muscle Disease.Antioxidants (Basel, Switzerland) · 2022Review
- Myostatin/Activin Receptor Ligands in Muscle and the Development Status of Attenuating Drugs.Endocrine reviews · 2022Review
- Myostatin Deficiency Enhances Antioxidant Capacity of Bovine Muscle via the SMAD-AMPK-G6PD Pathway.Oxidative medicine and cellular longevity · 2022Article
- Mitochondrial Function and Reactive Oxygen/Nitrogen Species in Skeletal Muscle.Frontiers in cell and developmental biology · 2022Review
- Mitochondria Homeostasis and Oxidant/Antioxidant Balance in Skeletal Muscle-Do Myokines Play a Role?Antioxidants (Basel, Switzerland) · 2021Review
- Regulation of Myostatin on the Growth and Development of Skeletal Muscle.Frontiers in cell and developmental biology · 2021Review
- Reactive Oxygen Species: Beyond Their Reactive Behavior.Neurochemical research · 2021Review
- MuRF1/TRIM63, Master Regulator of Muscle Mass.International journal of molecular sciences · 2020Review
- The Role of Nutri(epi)genomics in Achieving the Body's Full Potential in Physical Activity.Antioxidants (Basel, Switzerland) · 2020Review
- Angiotensin (1-7) Decreases Myostatin-Induced NF-κB Signaling and Skeletal Muscle Atrophy.International journal of molecular sciences · 2020Article
- Article
- Cancer Takes a Toll on Skeletal Muscle by Releasing Heat Shock Proteins-An Emerging Mechanism of Cancer-Induced Cachexia.Cancers · 2019Review
- Systems biology and network pharmacology of frailty reveal novel epigenetic targets and mechanisms.Scientific reports · 2019Article
- Upregulation of Heme Oxygenase-1 by Hemin Alleviates Sepsis-Induced Muscle Wasting in Mice.Oxidative medicine and cellular longevity · 2018Article
- Activin A induces skeletal muscle catabolism via p38β mitogen-activated protein kinase.Journal of cachexia, sarcopenia and muscle · 2017Article
- Matrix Metalloproteinase Responsive Delivery of Myostatin Inhibitors.Pharmaceutical research · 2017Article
Corrections and comments
- Correction · 2016-02-01Concerns/Issues about Data · Concerns/Issues about Image · Error in Image · Error in Text · Falsification/Fabrication of Data · Investigation by Company/Institution · Misconduct - Official Investigation(s) and/or Finding(s) · · Endocrine Society publishes with Oxford Academic Sudarsanareddy Lokireddy and Sandhya Sriram were the focus of an investigation. From Retraction Watch post: 'Sudarsanareddy Lokireddy — now a research fellow at Harvard Medical School —'admitted falsification,' a Research Integrity Officer at Nanyang Technological University in Singapore told us in December.'
- Erratum issuedCorrigendum.2016
Authors and funding
9 authors at 5 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Smad (Sma and Mad-related protein) 2/3 are downstream signaling molecules for TGF-β and myostatin (Mstn). Recently, Mstn was shown to induce reactive oxygen species (ROS) in skeletal muscle via canonical Smad3, nuclear factor-κB, and TNF-α pathway. However, mice lacking Smad3 display skeletal muscle atrophy due to increased Mstn levels. Hence, our aims were first to investigate whether Mstn induced muscle atrophy in Smad3(-/-) mice by increasing ROS and second to delineate Smad3-independent signaling mechanism for Mstn-induced ROS. Herein we show that Smad3(-/-) mice have increased ROS levels in skeletal muscle, and inactivation of Mstn in these mice partially ablates the oxidative stress. Furthermore, ROS induction by Mstn in Smad3(-/-) muscle was not via nuclear factor-κB (p65) signaling but due to activated p38, ERK MAPK signaling and enhanced IL-6 levels. Consequently, TNF-α, nicotinamide adenine dinucleotide phosphate oxidase, and xanthine oxidase levels were up-regulated, which led to an increase in ROS production in Smad3(-/-) skeletal muscle. The exaggerated ROS in the Smad3(-/-) muscle potentiated binding of C/EBP homology protein transcription factor to MuRF1 promoter, resulting in enhanced MuRF1 levels leading to muscle atrophy.
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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.