ArticleHuman molecular genetics2012
E2F transcription factor-1 deficiency reduces pathophysiology in the mouse model of Duchenne muscular dystrophy through increased muscle oxidative metabolism.
Article in Human molecular genetics, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 27 citations in OpenAlex.
- Downstream Pathways of Dystrophin Deficiency in Duchenne Muscular Dystrophy: Implications for Muscle Degeneration and Regeneration.Journal of cachexia, sarcopenia and muscle · 2026Review
- Molecular pathways involved in the control of contractile and metabolic properties of skeletal muscle fibers as potential therapeutic targets for Duchenne muscular dystrophy.Frontiers in physiology · 2024Review
- Characterization of pig skeletal muscle transcriptomes in response to low temperature.Veterinary medicine and science · 2023Article
- Beneficial Role of Exercise in the Modulation ofAntioxidants (Basel, Switzerland) · 2021Review
- Article
- Mitochondrial Dysfunction Is an Early Consequence of Partial or Complete Dystrophin Loss inFrontiers in physiology · 2020Article
- Role and Significance of Circulating Biomarkers: miRNA and E2F1 mRNA Expression and Their Association with Type-2 Diabetic Complications.International journal of endocrinology · 2020Article
- E2F1, a Novel Regulator of Metabolism.Frontiers in endocrinology · 2017Review
- Increased mitochondrial function downstream from KDM5A histone demethylase rescues differentiation in pRB-deficient cells.Genes & development · 2015Article
- Emerging links between E2F control and mitochondrial function.Cancer research · 2015Review
- E2F1 is a novel fibrogenic gene that regulates cholestatic liver fibrosis through the Egr-1/SHP/EID1 network.Hepatology (Baltimore, Md.) · 2014Article
- Resveratrol induces expression of the slow, oxidative phenotype in mdx mouse muscle together with enhanced activity of the SIRT1-PGC-1α axis.American journal of physiology. Cell physiology · 2014Article
- Pharmacologic management of Duchenne muscular dystrophy: target identification and preclinical trials.ILAR journal · 2014Review
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Authors and funding
8 authors at 4 institutions in 1 country.
Funding
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Abstract
E2F1 deletion leads to increased mitochondrial number and function, increased body temperature in response to cold and increased resistance to fatigue with exercise. Since E2f1-/- mice show increased muscle performance, we examined the effect of E2f1 genetic inactivation in the mdx background, a mouse model of Duchenne muscular dystrophy (DMD). E2f1-/-;mdx mice demonstrated a strong reduction of physiopathological signs of DMD, including preservation of muscle structure, decreased inflammatory profile, increased utrophin expression, resulting in better endurance and muscle contractile parameters, comparable to normal mdx mice. E2f1 deficiency in the mdx genetic background increased the oxidative metabolic gene program, mitochondrial activity and improved muscle functions. Interestingly, we observed increased E2F1 protein levels in DMD patients, suggesting that E2F1 might represent a promising target for the treatment of DMD.
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