ArticleScientific reports2017
Long-term PGC1β overexpression leads to apoptosis, autophagy and muscle wasting.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
What it found
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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.
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Who cites it
11 citing papers in PubMed, 14 citations in OpenAlex.
- Senescence dynamics define therapeutic windows for Duchenne muscular dystrophy in DBA/2-mdx mice.Skeletal muscle · 2026Article
- NEDD4 enhances bone‑tendon healing in rotator cuff tears by reducing fatty infiltration.Molecular medicine reports · 2025Article
- Mitochondrial Quality Control: A New Perspective in Skeletal Muscle Dysfunction of Chronic Obstructive Pulmonary Disease.Aging and disease · 2024Review
- The Role of theAnimals : an open access journal from MDPI · 2024Article
- Main Pathogenic Mechanisms and Recent Advances in COPD Peripheral Skeletal Muscle Wasting.International journal of molecular sciences · 2023Review
- PGC-1β maintains mitochondrial metabolism and restrains inflammatory gene expression.Scientific reports · 2022Article
- Changes of Gene Expression Patterns of Muscle Pathophysiology-Related Transcription Factors During Denervated Muscle Atrophy.Frontiers in physiology · 2022Article
- Transcriptional changes in muscle of hibernating arctic ground squirrels (Urocitellus parryii): implications for attenuation of disuse muscle atrophy.Scientific reports · 2020Article
- Reduced skeletal muscle independently predicts 1-year aggravated joint destruction in patients with rheumatoid arthritis.Therapeutic advances in musculoskeletal disease · 2020Article
- The Marine DinoflagellateMarine drugs · 2018Article
- microRNA-378 promotes autophagy and inhibits apoptosis in skeletal muscle.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
Corrections and comments
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Authors and funding
12 authors at 4 institutions in 1 country.
Funding
Abstract
Skeletal muscle wasting is prevalent in many chronic diseases, necessitating inquiries into molecular regulation of muscle mass. Nuclear receptor co-activator peroxisome proliferator-activated receptor co-activator 1 alpha (PGC1α) and its splice variant PGC1α4 increase skeletal muscle mass. However, the effect of the other PGC1 sub-type, PGC1β, on muscle size is unclear. In transgenic mice selectively over-expressing PGC1β in the skeletal muscle, we have found that PGC1β progressively decreases skeletal muscle mass predominantly associated with loss of type 2b fast-twitch myofibers. Paradoxically, PGC1β represses the ubiquitin-proteolysis degradation pathway genes resulting in ubiquitinated protein accumulation in muscle. However, PGC1β overexpression triggers up-regulation of apoptosis and autophagy genes, resulting in robust activation of these cell degenerative processes, and a concomitant increase in muscle protein oxidation. Concurrently, PGC1β up-regulates apoptosis and/or autophagy transcriptional factors such as E2f1, Atf3, Stat1, and Stat3, which may be facilitating myopathy. Therefore, PGC1β activation negatively affects muscle mass over time, particularly fast-twitch muscles, which should be taken into consideration along with its known aerobic effects in the skeletal muscle.
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Registered trials
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