ReviewEuropean journal of applied physiology2019
Mitochondrial health and muscle plasticity after spinal cord injury.
Review in European journal of applied physiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
34 citing papers in PubMed, 57 citations in OpenAlex.
- Neuromuscular electrical stimulation resistance training enhances oxygen uptake and ventilatory efficiency independent of mitochondrial complexes after spinal cord injury: a randomized clinical trial.Journal of applied physiology (Bethesda, Md. : 1985) · 2021Trial
- Predictors of Ultrasound-Derived Muscle Thickness and Echo Intensity After Acute Incomplete Spinal Cord Injury During Inpatient Rehabilitation: An Exploratory Observational Cohort Study.Journal of clinical medicine · 2026Article
- Kainate-induced ATP release contributes to spinal excitotoxicity that is attenuated by purinergic blockade.Frontiers in neurology · 2026Article
- Functionalized nanozyme delivery of a KCC2-activator conjugate for the promotion of functional recovery after acute spinal cord injury.Materials today. Bio · 2025Article
- Hypoxia Conditioning for Load-Compromised Athletes: A Narrative Review Exploring Potential Applications in Injury and Disability Management.Sports medicine (Auckland, N.Z.) · 2025Review
- Identification of key genes associated with muscle atrophy after spinal cord injury and experimental verification in rats.Frontiers in immunology · 2025Article
- Low-frequency electrically induced exercise after spinal cord injury: Physiologic challenge to skeletal muscle and feasibility for long-term use.The journal of spinal cord medicine · 2024Article
- SPTLC3 Is Essential for Complex I Activity and Contributes to Ischemic Cardiomyopathy.Circulation · 2024Article
- Defective autophagy and autophagy activators in myasthenia gravis: a rare entity and unusual scenario.Autophagy · 2024Review
- The Effect of Glycine and N-Acetylcysteine on Oxidative Stress in the Spinal Cord and Skeletal Muscle After Spinal Cord Injury.Inflammation · 2024Article
- Article
- Neuromuscular disorders in women and men with spinal cord injury are associated with changes in muscle and tendon architecture.The journal of spinal cord medicine · 2023Article
- Mitochondrial dysfunction: roles in skeletal muscle atrophy.Journal of translational medicine · 2023Review
- Mechanism of skeletal muscle atrophy after spinal cord injury: A narrative review.Frontiers in nutrition · 2023Review
- Review
- Article
- How Does the Central Nervous System for Posture and Locomotion Cope With Damage-Induced Neural Asymmetry?Frontiers in systems neuroscience · 2022Review
- Pharmacologic approaches to prevent skeletal muscle atrophy after spinal cord injury.Current opinion in pharmacology · 2021Review
- The emerging role of circular RNAs in spinal cord injury.Journal of orthopaedic translation · 2021Review
- Effects of a Tailored Physical Activity Intervention on Cardiovascular Structure and Function in Individuals With Spinal Cord Injury.Neurorehabilitation and neural repair · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 5 institutions in 2 countries.
Funding
Abstract
Mitochondria are responsible for aerobic respiration and large-scale ATP production in almost all cells of the body. Their function is decreased in many neurodegenerative and cardiovascular disease states, in metabolic disorders such as type II diabetes and obesity, and as a normal component of aging. Disuse of skeletal muscle from immobilization or unloading triggers alterations of mitochondrial density and activity. Resultant mitochondrial dysfunction after paralysis, which precedes muscle atrophy, may augment subsequent release of reactive oxygen species leading to protein ubiquitination and degradation. Spinal cord injury is a unique form of disuse atrophy as there is a complete or partial disruption in tonic communication between the central nervous system (CNS) and skeletal muscle. Paralysis, unloading and disruption of CNS communication result in a rapid decline in skeletal muscle function and metabolic status with disruption in activity of peroxisome-proliferator-activated receptor-gamma co-activator 1 alpha and calcineurin, key regulators of mitochondrial health and function. External interventions, both acute and chronical with training using body-weight-assisted treadmill training or electrical stimulation have consistently demonstrated adaptations in skeletal muscle mitochondria, and expression of the genes and proteins required for mitochondrial oxidation of fats and carbohydrates to ATP, water, and carbon dioxide. The purpose of this mini-review is to highlight our current understanding as to how paralysis mechanistically triggers downstream regulation in mitochondrial density and activity and to discuss how mitochondrial dysfunction may contribute to skeletal muscle atrophy.
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What OpenQuestion holds
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.