ReviewBiochimica et biophysica acta2009
Mouse models of oxidative phosphorylation defects: powerful tools to study the pathobiology of mitochondrial diseases.
Review in Biochimica et biophysica acta, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 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
22 citing papers in PubMed, 37 citations in OpenAlex.
- Understanding coenzyme Q.Physiological reviews · 2024Review
- Disruption of mitochondrial energy metabolism is a putative pathogenesis of Diamond-Blackfan anemia.iScience · 2024Article
- Challenges and opportunities to bridge translational to clinical research for personalized mitochondrial medicine.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2024Review
- Parkin deficiency exacerbates fasting-induced skeletal muscle wasting in mice.NPJ Parkinson's disease · 2022Article
- The Diagnostic Approach to Mitochondrial Disorders in Children in the Era of Next-Generation Sequencing: A 4-Year Cohort Study.Journal of clinical medicine · 2021Article
- Kidney epithelial targeted mitochondrial transcription factor A deficiency results in progressive mitochondrial depletion associated with severe cystic disease.Kidney international · 2021Article
- Leigh Syndrome: A Tale of Two Genomes.Frontiers in physiology · 2021Review
- A Targeted Mutation Disrupting Mitochondrial Complex IV Function in Primary Afferent Neurons Leads to Pain Hypersensitivity Through P2YMolecular neurobiology · 2019Article
- Early detection of elevated lactate levels in a mitochondrial disease model using chemical exchange saturation transfer (CEST) and magnetic resonance spectroscopy (MRS) at 7T-MRI.Radiological physics and technology · 2019Article
- Nutritional Interventions for Mitochondrial OXPHOS Deficiencies: Mechanisms and Model Systems.Annual review of pathology · 2018Review
- Functional and Molecular Insights of Hydrogen Sulfide Signaling and Protein Sulfhydration.Journal of molecular biology · 2017Review
- A Metabolic Signature of Mitochondrial Dysfunction Revealed through a Monogenic Form of Leigh SyndromeCell reports · 2015Article
- A Drosophila model of mitochondrial disease caused by a complex I mutation that uncouples proton pumping from electron transfer.Disease models & mechanisms · 2014Article
- Turn up the power - pharmacological activation of mitochondrial biogenesis in mouse models.British journal of pharmacology · 2014Review
- Mitochondrial biogenesis: a therapeutic target for neurodevelopmental disorders and neurodegenerative diseases.Current pharmaceutical design · 2014Review
- Mouse models of mitochondrial complex I dysfunction.The international journal of biochemistry & cell biology · 2013Review
- A defect in the mitochondrial complex III, but not complex IV, triggers early ROS-dependent damage in defined brain regions.Human molecular genetics · 2012Article
- Metabolic control of mitochondrial biogenesis through the PGC-1 family regulatory network.Biochimica et biophysica acta · 2011Review
- Region-specific expression of mitochondrial complex I genes during murine brain development.PloS one · 2011Article
- Andropause and the development of cardiovascular disease presentation-more than an epi-phenomenon.Journal of geriatric cardiology : JGC · 2011Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Defects in the oxidative phosphorylation system (OXPHOS) are responsible for a group of extremely heterogeneous and pleiotropic pathologies commonly known as mitochondrial diseases. Although many mutations have been found to be responsible for OXPHOS defects, their pathogenetic mechanisms are still poorly understood. An important contribution to investigate the in vivo function of several mitochondrial proteins and their role in mitochondrial dysfunction, has been provided by mouse models. Thanks to their genetic and physiologic similarity to humans, mouse models represent a powerful tool to investigate the impact of pathological mutations on metabolic pathways. In this review we discuss the main mouse models of mitochondrial disease developed, focusing on the ones that directly affect the OXPHOS system.
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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.