ArticleSkeletal muscle2011
PPARδ regulates satellite cell proliferation and skeletal muscle regeneration.
Article in Skeletal muscle, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 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
38 citing papers in PubMed, 60 citations in OpenAlex.
- The role of mNaunyn-Schmiedeberg's archives of pharmacology · 2026Review
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- Mitonuclear Communication in Stem Cell Function.Cell proliferation · 2025Review
- Unveiling Key Genes and Crucial Pathways in Goose Muscle Satellite Cell Biology Through Integrated Transcriptomic and Metabolomic Analyses.International journal of molecular sciences · 2025Article
- Metabolic regulation in adult and aging skeletal muscle stem cells.Genes & development · 2025Review
- Review
- Integration of ATAC-Seq and RNA-Seq Analysis to Identify Key Genes in the Longissimus Dorsi Muscle Development of the Tianzhu White Yak.International journal of molecular sciences · 2023Article
- Nuclear receptors as potential therapeutic targets in peripheral arterial disease and related myopathy.The FEBS journal · 2023Review
- Juvenile zebrafish (Danio rerio) are able to recover from lordosis.Scientific reports · 2022Article
- Identification of Key Genes and Biological Pathways Associated with Skeletal Muscle Maturation and Hypertrophy inAnimals : an open access journal from MDPI · 2022Article
- Molecular mechanisms of exercise contributing to tissue regeneration.Signal transduction and targeted therapy · 2022Review
- Skeletal Muscle Regeneration in Cardiotoxin-Induced Muscle Injury Models.International journal of molecular sciences · 2022Review
- Skeletal Muscle Metabolic Alternation Develops Sarcopenia.Aging and disease · 2022Review
- Nuclear Receptors in Energy Metabolism.Advances in experimental medicine and biology · 2022Article
- Mitochondrial dysfunction and consequences in calpain-3-deficient muscle.Skeletal muscle · 2020Article
- Degenerative and regenerative pathways underlying Duchenne muscular dystrophy revealed by single-nucleus RNA sequencing.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- PPARs and Microbiota in Skeletal Muscle Health and Wasting.International journal of molecular sciences · 2020Review
- Bioenergetic-active materials enhance tissue regeneration by modulating cellular metabolic state.Science advances · 2020Article
- PPARγ Controls Ectopic Adipogenesis and Cross-Talks with Myogenesis During Skeletal Muscle Regeneration.International journal of molecular sciences · 2018Article
- PPARβ/δ: Linking Metabolism to Regeneration.International journal of molecular sciences · 2018Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Peroxisome proliferator-activated receptors (PPARs) are a class of nuclear receptors that play important roles in development and energy metabolism. Whereas PPARδ has been shown to regulate mitochondrial biosynthesis and slow-muscle fiber types, its function in skeletal muscle progenitors (satellite cells) is unknown. Since constitutive mutation of Pparδ leads to embryonic lethality, we sought to address this question by conditional knockout (cKO) of Pparδ using Myf5-Cre/Pparδflox/flox alleles to ablate PPARδ in myogenic progenitor cells. Although Pparδ-cKO mice were born normally and initially displayed no difference in body weight, muscle size or muscle composition, they later developed metabolic syndrome, which manifested as increased body weight and reduced response to glucose challenge at age nine months. Pparδ-cKO mice had 40% fewer satellite cells than their wild-type littermates, and these satellite cells exhibited reduced growth kinetics and proliferation in vitro. Furthermore, regeneration of Pparδ-cKO muscles was impaired after cardiotoxin-induced injury. Gene expression analysis showed reduced expression of the Forkhead box class O transcription factor 1 (FoxO1) gene in Pparδ-cKO muscles under both quiescent and regenerating conditions, suggesting that PPARδ acts through FoxO1 in regulating muscle progenitor cells. These results support a function of PPARδ in regulating skeletal muscle metabolism and insulin sensitivity, and they establish a novel role of PPARδ in muscle progenitor cells and postnatal muscle regeneration.
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.