ArticleNeurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology2013
ANT1 is reduced in sporadic inclusion body myositis.
Article in Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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5 citing papers in PubMed, 9 citations in OpenAlex.
- ANT1 Deficiency Impairs Macrophage Metabolism and Migration, Protecting Against Emphysema in Chronic Obstructive Pulmonary Disease.American journal of respiratory cell and molecular biology · 2025Article
- Alternations of NF-κB Signaling by Natural Compounds in Muscle-Derived Cancers.International journal of molecular sciences · 2023Review
- DISCUSSING ANT1 ROLE IN AMYOTROPHIC LATERAL SCLEROSIS PATHOGENESIS.Innovations in clinical neuroscience · 2018Article
- Inclusion body myositis - pathomechanism and lessons from genetics.Open medicine (Warsaw, Poland) · 2015Review
- Phenotypic rescue of a Drosophila model of mitochondrial ANT1 disease.Disease models & mechanisms · 2014Article
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9 authors at 1 institution in 1 country.
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Abstract
To investigate ANT1 and NF-κB expression in inclusion body myositis (IBM) muscle and to verify their possible roles in the pathogenesis of the disease, we collected muscle samples from five patients with IBM, polimyositis (PM) and controls. p65 form of NF-κB was analyzed using immunocytochemistry, Western blot and EMSA. Western blot of ANT1 was performed and confirmed by gene expression study. Mann-Whitney test was used for groups comparisons. NF-κB (p65) was found over-expressed both with western blot and EMSA, either in IBM or PM patients versus controls (p < 0.01). Expression of ANT1 were lower in IBM samples versus both PM and controls (p < 0.01). ANT1 reduction and NF-κB over-expression in IBM muscle could explain the lack of apoptosis in such disease. Normal ANT1 expression in PM could be related to the scarcity of mitochondrial abnormalities in the disease, but it could also suggest that these two conditions diverge in activating different anti-apoptotic pathways.
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