ArticleTobacco induced diseases2017
Tumor necrosis factor-like weak inducer of apoptosis regulates quadriceps muscle atrophy and fiber-type alteration in a rat model of chronic obstructive pulmonary disease.
Article in Tobacco induced diseases, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 1 of them a synthesis that pooled it.
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Who cites it
8 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Do dietary supplements prevent loss of muscle mass and strength during muscle disuse? A systematic review and meta-analysis of randomized controlled trials.Frontiers in nutrition · 2023Pooled it
- Main Pathogenic Mechanisms and Recent Advances in COPD Peripheral Skeletal Muscle Wasting.International journal of molecular sciences · 2023Review
- Amelioration of cancer cachexia with preemptive administration of tumor necrosis factor-α blocker.Journal of clinical biochemistry and nutrition · 2022Article
- Putative MicroRNA-mRNA Networks Upon Mdfi Overexpression in C2C12 Cell Differentiation and Muscle Fiber Type Transformation.Frontiers in molecular biosciences · 2021Article
- The BRD4 inhibitor JQ1 protects against chronic obstructive pulmonary disease in mice by suppressing NF-κB activation.Histology and histopathology · 2021Article
- Mdfi Promotes C2C12 Cell Differentiation and Positively Modulates Fast-to-Slow-Twitch Muscle Fiber Transformation.Frontiers in cell and developmental biology · 2021Article
- Bufei Jianpi Formula Improves Mitochondrial Function and Suppresses Mitophagy in Skeletal Muscle via the Adenosine Monophosphate-Activated Protein Kinase Pathway in Chronic Obstructive Pulmonary Disease.Frontiers in pharmacology · 2020Article
- A Novel Murine Chronic Obstructive Pulmonary Disease Model and the Pathogenic Role of MicroRNA-21.Frontiers in physiology · 2018Article
Corrections and comments
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Authors and funding
5 authors.
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No grant is acknowledged in the PubMed record.
Abstract
backgroundIn chronic obstructive pulmonary disease (COPD), weakness and muscle mass loss of the quadriceps muscle has been demonstrated to predict survival and mortality rates of patients. Tumor necrosis factor (TNF)-like weak inducer of apoptosis (TWEAK), as a member of the TNF superfamily, has recently been identified as a key regulator of skeletal muscle wasting and metabolic dysfunction. So our aim was to study the role of TWEAK during quadriceps muscle atrophy and fiber-type transformation in COPD model rats and its possible pathway.
methodsForty-four healthy male adult Wistar rats were randomly divided into two groups: A normal control group (
resultsCompared with controls, COPD model rats exhibited significantly lower quadriceps muscle weight (
conclusionsCollectively these data suggest that increased levels of TWEAK may lead to skeletal muscle atrophy and fiber-type alteration, which in turn may be associated with activation of the ubiquitin-proteasome pathway, involving NF-κB, MuRF1 and PGC-1α as potential regulatory factors. These preliminary results in rats suggest that TWEAK may be a therapeutic target for the treatment of muscle atrophy in COPD.
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