ArticleThe Journal of biological chemistry2012
Mitochondrial dysfunction in skeletal muscle of amyloid precursor protein-overexpressing mice.
Article in The Journal of biological chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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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.
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Who cites it
18 citing papers in PubMed, 33 citations in OpenAlex.
- Energy metabolism dysregulation in idiopathic inflammatory myopathies: mechanisms and therapeutic implications.Frontiers in immunology · 2026Review
- Effects and mechanisms of APP and its cleavage product Aβ in the comorbidity of sarcopenia and Alzheimer's disease.Frontiers in aging neuroscience · 2024Review
- Mitochondrial defects in sporadic inclusion body myositis-causes and consequences.Frontiers in cell and developmental biology · 2024Review
- DNA methylation of insulin signaling pathways is associated with HOMA2-IR in primary myoblasts from older adults.Skeletal muscle · 2023Article
- The Emerging Role of Mitochondrial Dysfunction in the Pathogenesis of Idiopathic Inflammatory Myopathies.Rambam Maimonides medical journal · 2023Review
- APP in the Neuromuscular Junction for the Development of Sarcopenia and Alzheimer's Disease.International journal of molecular sciences · 2023Review
- Amyloid aggregates of the deubiquitinase OTUB1 are neurotoxic, suggesting that they contribute to the development of Parkinson's disease.The Journal of biological chemistry · 2020Article
- Neurochemical Aspects of Alzheimer's Disease and Movement Disturbances: A Theory of β-Amyloid and τ-Protein.American journal of Alzheimer's disease and other dementias · 2018Article
- Risk factors and disease mechanisms in myositis.Nature reviews. Rheumatology · 2018Review
- Treadmill exercise ameliorates the regulation of energy metabolism in skeletal muscle of NSE/PS2mtransgenic mice with Alzheimer's disease.Journal of exercise nutrition & biochemistry · 2017Article
- Age-dependent uncoupling of mitochondria from Ca2⁺ release units in skeletal muscle.Oncotarget · 2015Article
- Age-dependent biochemical dysfunction in skeletal muscle of triple-transgenic mouse model of Alzheimer`s disease.Current Alzheimer research · 2015Article
- Aberrant cell cycle reentry in human and experimental inclusion body myositis and polymyositis.Human molecular genetics · 2014Article
- Mitochondrial oxygen consumption deficits in skeletal muscle isolated from an Alzheimer's disease-relevant murine model.BMC neuroscience · 2014Article
- Primary over-expression of AβPP in muscle does not lead to the development of inclusion body myositis in a new lineage of the MCK-AβPP transgenic mouse.International journal of experimental pathology · 2013Article
- Divergent modification of low-dose ⁵⁶Fe-particle and proton radiation on skeletal muscle.Radiation research · 2013Article
- Interactions between sarco-endoplasmic reticulum and mitochondria in cardiac and skeletal muscle - pivotal roles in Ca²⁺ and reactive oxygen species signaling.Journal of cell science · 2013Review
- Mutant amyloid precursor protein differentially alters adipose biology under obesogenic and non-obesogenic conditions.PloS one · 2012Article
Corrections and comments
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Authors and funding
7 authors at 5 institutions in 2 countries.
Funding
Abstract
Inclusion body myositis, the most common muscle disorder in the elderly, is partly characterized by abnormal expression of amyloid precursor protein (APP) and intracellular accumulation of its proteolytic fragments collectively known as β-amyloid. The present study examined the effects of β-amyloid accumulation on mitochondrial structure and function of skeletal muscle from transgenic mice (MCK-βAPP) engineered to accumulate intramyofiber β-amyloid. Electron microscopic analysis revealed that a large fraction of myofibers from 2-3-month-old MCK-βAPP mice contained numerous, heterogeneous alterations in mitochondria, and other cellular organelles. [(1)H-decoupled](13)C NMR spectroscopy showed a substantial reduction in TCA cycle activity and indicated a switch from aerobic to anaerobic glucose metabolism in the MCK-βAPP muscle. Isolated muscle fibers from the MCK-βAPP mice also exhibited a reduction in cytoplasmic pH, an increased rate of ROS production, and a partially depolarized plasmalemma. Treatment of MCK-βAPP muscle cells with Ru360, a mitochondrial Ca(2+) uniporter antagonist, reversed alterations in the plasmalemmal membrane potential (V(m)) and pH. Consistent with altered redox state of the cells, treatment of MCK-βAPP muscle cells with glutathione reversed the effects of β-amyloid accumulation on Ca(2+) transient amplitudes. We conclude that structural and functional alterations in mitochondria precede the reported appearance of histopathological and clinical features in the MCK-βAPP mice and may represent key early events in the pathogenesis of inclusion body myositis.
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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.