ReviewF1000Research2019
Mitochondrial dysregulation and muscle disuse atrophy.
Review in F1000Research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 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
49 citing papers in PubMed.
- Amino acid supplementation accelerates resolution of exercise-induced phagocyte infiltration in human skeletal muscle.Journal of the International Society of Sports Nutrition · 2025Trial
- Mitochondrial ROS dyshomeostasis: a key driver of accelerated supraspinatus atrophy after rotator cuff injury.Frontiers in physiology · 2026Review
- HCMV immediate-early protein IE2 induces neurotoxicity and hearing loss by disrupting TSC2-mTOR signaling and metabolic homeostasis.Journal of neuroinflammation · 2025Article
- Transcriptomic time course of skeletal muscle disuse and rehabilitation in middle-aged adults.Physiological reports · 2025Article
- Article
- Chestnut (Nutrients · 2025Article
- Antioxidant Status in Children with Neurogenic Bladder.Children (Basel, Switzerland) · 2025Article
- High-Resolution Tracking of Aging-Related Small Molecules: Bridging Pollutant Exposure, Brain Aging Mechanisms, and Detection Innovations.Biosensors · 2025Review
- Network Pharmacology Combined with Experimental Validation to Investigate the Effects and Mechanisms of Aucubin on Aging-Related Muscle Atrophy.International journal of molecular sciences · 2025Article
- Fostering tissue engineering and regenerative medicine to treat musculoskeletal disorders in bone and muscle.Bioactive materials · 2024Review
- Identifying the potential therapeutic effects of miR‑6516 on muscle disuse atrophy.Molecular medicine reports · 2024Article
- Pathophysiological changes of muscle after ischemic stroke: a secondary consequence of stroke injury.Neural regeneration research · 2024Review
- Spinal cord abnormal autophagy and mitochondria energy metabolism are modified by swim training in SOD1-G93A mice.Journal of molecular medicine (Berlin, Germany) · 2024Article
- Type 2 diabetes mellitus related sarcopenia: a type of muscle loss distinct from sarcopenia and disuse muscle atrophy.Frontiers in endocrinology · 2024Review
- Factors, mechanisms and improvement methods of muscle strength loss.Frontiers in cell and developmental biology · 2024Review
- PRMT5 links lipid metabolism to contractile function of skeletal muscles.EMBO reports · 2023Article
- Melatonin Improves Skeletal Muscle Structure and Oxidative Phenotype by Regulating Mitochondrial Dynamics and Autophagy in Zücker Diabetic Fatty Rat.Antioxidants (Basel, Switzerland) · 2023Article
- The Role of Mitochondria in Mediation of Skeletal Muscle Repair.Muscles (Basel, Switzerland) · 2023Review
- Human Neuromuscular Junction on a Chip: Impact of Amniotic Fluid Stem Cell Extracellular Vesicles on Muscle Atrophy and NMJ Integrity.International journal of molecular sciences · 2023Article
- Pathophysiological Aspects of Muscle Atrophy and Osteopenia Induced by Chronic Constriction Injury (CCI) of the Sciatic Nerve in Rats.International journal of molecular sciences · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
It is well established that mitochondria play a critical role in the metabolic and physiological adaptation of skeletal muscle to enhanced contractile activity. Several redox-sensitive signaling pathways such as PGC-1α, AMPK, IGF/Akt/mTOR, SIRT, NFκB, and FoxO are involved with extensive crosstalk to regulate vital cellular functions such as mitochondrial biogenesis, mitochondrial fusion and fission dynamics, autophagy/mitophagy, and apoptosis under altered demand and stress. However, when muscles cease contraction, such as during immobilization and denervation, mitochondria undergo a series of detrimental changes characterized by downregulation of PGC-1α and antioxidant defense, increased ROS generation, activated FoxO, NFκB, and inflammation, enhanced ubiquitination, and finally mitophagy and apoptotic cascades. The phenotypic outcome of the discord of mitochondrial homeostasis is elevated proteolysis and muscle atrophy. The demonstration that PGC-1α overexpression via transgene or
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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.