ReviewInternational journal of molecular sciences2022
Remarks on Mitochondrial Myopathies.
Review in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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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
9 citing papers in PubMed, 14 citations in OpenAlex.
- Mitochondria in SARS-CoV-2 infection: Immune interactions and molecular approaches in the Post COVID-19 condition.Genetics and molecular biology · 2026Article
- Navigating gastrointestinal challenges in genetic myopathies: Diagnostic insights and future directions.World journal of methodology · 2025Article
- Clinical and Pathological Features of Flexural Deformities Associated with Myopathies in Foals.Veterinary sciences · 2025Article
- Plasma Metabolite Profiles Between In-Center Daytime Extended-Hours and Conventional Hemodialysis.Kidney360 · 2025Article
- Advances in the treatment of lower-extremity ischemia-reperfusion injury.Frontiers in pharmacology · 2025Review
- Subcellular NADNature metabolism · 2024Article
- Review
- A clinical approach to diagnosis and management of mitochondrial myopathies.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2024Review
- Interactions of mitochondrial and skeletal muscle biology in mitochondrial myopathy.The Biochemical journal · 2023Review
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mitochondrial myopathies represent a heterogeneous group of diseases caused mainly by genetic mutations to proteins that are related to mitochondrial oxidative metabolism. Meanwhile, a similar etiopathogenetic mechanism (i.e., a deranged oxidative phosphorylation and a dramatic reduction of ATP synthesis) reveals that the evolution of these myopathies show significant differences. However, some physiological and pathophysiological aspects of mitochondria often reveal other potential molecular mechanisms that could have a significant pathogenetic role in the clinical evolution of these disorders, such as: i. a deranged ROS production both in term of signaling and in terms of damaging molecules; ii. the severe modifications of nicotinamide adenine dinucleotide (NAD)+/NADH, pyruvate/lactate, and α-ketoglutarate (α-KG)/2- hydroxyglutarate (2-HG) ratios. A better definition of the molecular mechanisms at the basis of their pathogenesis could improve not only the clinical approach in terms of diagnosis, prognosis, and therapy of these myopathies but also deepen the knowledge of mitochondrial medicine in general.
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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.