ArticleScientific reports2017
Pharmacological inhibition of REV-ERB stimulates differentiation, inhibits turnover and reduces fibrosis in dystrophic muscle.
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 25 papers.
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Who cites it
25 citing papers in PubMed, 46 citations in OpenAlex.
- Rev-erb-α in Skeletal Muscle Adaptation: Integrating Circadian Control Mechanisms and Exercise Dynamic Responses.Journal of cellular physiology · 2026Review
- The Small Molecule SR8278 Inhibits Cell Proliferation Independent of the REV-ERB Nuclear Receptor Proteins in Human Keratinocytes.Biomolecules · 2026Article
- Mature Schwann Cells Derived From Human Induced Pluripotent Stem Cells Promote Peripheral Nerve Regeneration In Vivo.Neuroscience insights · 2026Article
- Targeting nuclear receptors in muscular dystrophies and regenerative myogenesis.Frontiers in cell and developmental biology · 2026Review
- Time to Reset: The Interplay Between Circadian Rhythms and Redox Homeostasis in Skeletal Muscle Ageing and Systemic Health.Antioxidants (Basel, Switzerland) · 2025Review
- Regulation of Stemness by NR1D2 in Colorectal Cancer.Biomedicines · 2025Article
- Circadian Clock in Muscle Disease Etiology and Therapeutic Potential for Duchenne Muscular Dystrophy.International journal of molecular sciences · 2024Review
- Mechanism of antagonist ligand binding to REV-ERBα.Scientific reports · 2024Article
- Targeting NR1D1 in organ injury: challenges and prospects.Military Medical Research · 2023Review
- Nuclear receptors as potential therapeutic targets in peripheral arterial disease and related myopathy.The FEBS journal · 2023Review
- Targeted screening and identification of chlorhexidine as a pro-myogenic circadian clock activator.Stem cell research & therapy · 2023Article
- Role of Circadian Transcription Factor Rev-Erb in Metabolism and Tissue Fibrosis.International journal of molecular sciences · 2022Review
- Article
- Sinapic Acid Ameliorates REV-ERB α Modulated Mitochondrial Fission against MPTP-Induced Parkinson's Disease Model.Biomolecules & therapeutics · 2022Article
- The role of REV-ERB in NASH.Acta pharmacologica Sinica · 2022Article
- The nuclear receptor REV-ERBα is implicated in the alteration of β-cell autophagy and survival under diabetogenic conditions.Cell death & disease · 2022Article
- Muscle mitochondrial remodeling by intermittent glucocorticoid drugs requires an intact circadian clock and muscle PGC1α.Science advances · 2022Article
- Down-regulation of BMAL1 by MiR-494-3p Promotes Hepatocellular Carcinoma Growth and Metastasis by Increasing GPAM-mediated Lipid Biosynthesis.International journal of biological sciences · 2022Article
- Rev-erbα exacerbates hepatic steatosis in alcoholic liver diseases through regulating autophagy.Cell & bioscience · 2021Article
- A KDM4-DBC1-SIRT1 Axis Contributes to TGF-b Induced Mesenchymal Transition of Intestinal Epithelial Cells.Frontiers in cell and developmental biology · 2021Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Duchenne muscular dystrophy (DMD) is a debilitating X-linked disorder that is fatal. DMD patients lack the expression of the structural protein dystrophin caused by mutations within the DMD gene. The absence of functional dystrophin protein results in excessive damage from normal muscle use due to the compromised structural integrity of the dystrophin associated glycoprotein complex. As a result, DMD patients exhibit ongoing cycles of muscle destruction and regeneration that promote inflammation, fibrosis, mitochondrial dysfunction, satellite cell (SC) exhaustion and loss of skeletal and cardiac muscle function. The nuclear receptor REV-ERB suppresses myoblast differentiation and recently we have demonstrated that the REV-ERB antagonist, SR8278, stimulates muscle regeneration after acute injury. Therefore, we decided to explore whether the REV-ERB antagonist SR8278 could slow the progression of muscular dystrophy. In mdx mice SR8278 increased lean mass and muscle function, and decreased muscle fibrosis and muscle protein degradation. Interestingly, we also found that SR8278 increased the SC pool through stimulation of Notch and Wnt signaling. These results suggest that REV-ERB is a potent target for the treatment of DMD.
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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.