ReviewAntioxidants (Basel, Switzerland)2020
The Impact of Mitochondrial Deficiencies in Neuromuscular Diseases.
Review in Antioxidants (Basel, Switzerland), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 44 citations in OpenAlex.
- A Unified Framework for Spinal Cord Injury Repair: Metabolic-Nutritional Microenvironment Remodeling, Immune Modulation, and Neural Regeneration.Molecular neurobiology · 2026Review
- Shifting the Balance: Mitochondrial Heteroplasmy as a Driver of Cardiac Disease.Circulation research · 2026Review
- Protein arginine methyltransferases coordinate mitochondrial stress adaptation and neuromuscular function.Experimental & molecular medicine · 2026Review
- Beyond Membrane Remodeling: Organelle Crosstalk and Convergent Pathology in Centronuclear Myopathy.Muscles (Basel, Switzerland) · 2026Review
- Continuous glucose monitoring-derived glycemic variability and low skeletal muscle mass in middle-aged and older adults with type 2 diabetes mellitus: an analysis using AWGS 2025 criteria.Diabetology & metabolic syndrome · 2026Article
- Targeting mitochondrial quality control: Ginsenoside Rg1 as a therapeutic candidate for neuromuscular diseases.Journal of ginseng research · 2026Review
- Navigating gastrointestinal challenges in genetic myopathies: Diagnostic insights and future directions.World journal of methodology · 2025Article
- Amyotrophic Lateral Sclerosis With Concurrent LHON-associated m.14484T>C Mutation: A Case Report and Literature Review.Revista de neurologia · 2025Review
- PRMT1 (protein arginine methyltransferase 1) is essential for neuromuscular junction and mitochondrial homeostasis via mitophagy regulation.Autophagy · 2025Article
- A Review of Pathophysiology, Molecular Mechanisms, and Omics Approaches of Spinal Cord Injury.International journal of molecular sciences · 2025Review
- Serum chitotriosidase-1 (CHIT1) as candidate biomarker for mitochondriopathies.Journal of neurology · 2025Article
- Comparative genetic diagnostic evaluation of pediatric neuromuscular diseases in a consanguineous population.Scientific reports · 2025Article
- Mechanistic insights into Nrf2-driven pathogenesis and therapeutic targeting in spinal cord injury.Frontiers in immunology · 2025Review
- Fibromyalgia diagnosis from a multi-omics approach: a gut feeling.Frontiers in microbiology · 2025Article
- Microglial pyroptosis as a therapeutic target after traumatic spinal cord injury: current progress and future directions.Frontiers in immunology · 2025Review
- Therapeutic strategies to modulate gut microbial health: Approaches for sarcopenia management.Histology and histopathology · 2024Review
- Review
- Targeting mitochondrial CaThe Journal of physiology · 2024Review
- External damp environment aggravates diarrhea in spleen deficiency and dampness syndrome in mice: involvement of small intestinal contents microbiota, energy metabolism, gastrointestinal and fluid functions.Frontiers in cellular and infection microbiology · 2024Article
- Diaphragm Fatigue in SMNΔ7 Mice and Its Molecular Determinants: An Underestimated Issue.International journal of molecular sciences · 2023Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Neuromuscular diseases (NMDs) are a heterogeneous group of acquired or inherited rare disorders caused by injury or dysfunction of the anterior horn cells of the spinal cord (lower motor neurons), peripheral nerves, neuromuscular junctions, or skeletal muscles leading to muscle weakness and waste. Unfortunately, most of them entail serious or even fatal consequences. The prevalence rates among NMDs range between 1 and 10 per 100,000 population, but their rarity and diversity pose difficulties for healthcare and research. Some molecular hallmarks are being explored to elucidate the mechanisms triggering disease, to set the path for further advances. In fact, in the present review we outline the metabolic alterations of NMDs, mainly focusing on the role of mitochondria. The aim of the review is to discuss the mechanisms underlying energy production, oxidative stress generation, cell signaling, autophagy, and inflammation triggered or conditioned by the mitochondria. Briefly, increased levels of inflammation have been linked to reactive oxygen species (ROS) accumulation, which is key in mitochondrial genomic instability and mitochondrial respiratory chain (MRC) dysfunction. ROS burst, impaired autophagy, and increased inflammation are observed in many NMDs. Increasing knowledge of the etiology of NMDs will help to develop better diagnosis and treatments, eventually reducing the health and economic burden of NMDs for patients and healthcare systems.
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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.