ArticleClinical and translational science2013
Differential gene expression reveals mitochondrial dysfunction in an imprinting center deletion mouse model of Prader-Willi syndrome.
Article in Clinical and translational science, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 27 citations in OpenAlex.
- Targeting Mitochondria for Postoperative Cognitive Dysfunction: From Mechanisms to Therapeutics.Molecular neurobiology · 2026Review
- Characterization of Circulating Protein Profiles in Individuals with Prader-Willi Syndrome and Individuals with Non-Syndromic Obesity.Journal of clinical medicine · 2024Article
- Evidence for parent-of-origin effects in autism spectrum disorder: a narrative review.Journal of applied genetics · 2023Review
- Associations between Oxidant/Antioxidant Status and Circulating Adipokines in Non-Obese Children with Prader-Willi Syndrome.Antioxidants (Basel, Switzerland) · 2023Article
- Paternal preconceptional diet enriched with n-3 polyunsaturated fatty acids affects offspring brain function in mice.Frontiers in nutrition · 2022Article
- Prader-Willi syndrome: an update on obesity and endocrine problems.Annals of pediatric endocrinology & metabolism · 2021Article
- Abnormalities of synaptic mitochondria in autism spectrum disorder and related neurodevelopmental disorders.Journal of molecular medicine (Berlin, Germany) · 2021Review
- Mitochondrial Dysfunction: A Common Denominator in Neurodevelopmental Disorders?Developmental neuroscience · 2021Review
- Interaction of melatonin and Bmal1 in the regulation of PI3K/AKT pathway components and cellular survival.Scientific reports · 2019Article
- Preclinical Testing in Translational Animal Models of Prader-Willi Syndrome: Overview and Gap Analysis.Molecular therapy. Methods & clinical development · 2019Review
- Genotype-Phenotype Relationships and Endocrine Findings in Prader-Willi Syndrome.Frontiers in endocrinology · 2019Review
- Preliminary observations of mitochondrial dysfunction in Prader-Willi syndrome.American journal of medical genetics. Part A · 2018Article
- Article
- Oxidative Stress in Cancer-Prone Genetic Diseases in Pediatric Age: The Role of Mitochondrial Dysfunction.Oxidative medicine and cellular longevity · 2016Review
- Loss of inherited genomic imprints in mice leads to severe disruption in placental lipid metabolism.Placenta · 2015Article
- Birth seasonality in Korean Prader-Willi syndrome with chromosome 15 microdeletion.Annals of pediatric endocrinology & metabolism · 2015Article
Corrections and comments
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Authors and funding
11 authors at 5 institutions in 2 countries.
Funding
Abstract
Prader-Willi syndrome (PWS) is a genetic disorder caused by deficiency of imprinted gene expression from the paternal chromosome 15q11-15q13 and clinically characterized by neonatal hypotonia, short stature, cognitive impairment, hypogonadism, hyperphagia, morbid obesity, and diabetes. Previous clinical studies suggest that a defect in energy metabolism may be involved in the pathogenesis of PWS. We focused our attention on the genes associated with energy metabolism and found that there were 95 and 66 mitochondrial genes differentially expressed in PWS muscle and brain, respectively. Assessment of enzyme activities of mitochondrial oxidative phosphorylation complexes in the brain, heart, liver, and muscle were assessed. We found the enzyme activities of the cardiac mitochondrial complexes II+III were up-regulated in the PWS imprinting center deletion mice compared to the wild-type littermates. These studies suggest that differential gene expression, especially of the mitochondrial genes may contribute to the pathophysiology of PWS.
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Registered trials
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