ReviewPhysiological reports2024
Unraveling the causes of sarcopenia: Roles of neuromuscular junction impairment and mitochondrial dysfunction.
Review in Physiological reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
32 citing papers in PubMed, 1 synthesis or guideline pooled it, 33 citations in OpenAlex.
- Pooled it
- The multiple composite risk index estimates the risks of sarcopenia and comorbidities: unveiling the role of oxidative balance score.Annals of medicine · 2026Article
- Review
- Effects of Traditional Chinese Mind-Body Exercise on Physical Function in Older Adults with Sarcopenia and Frailty: A Meta-Analysis of Randomized Controlled Trials.Healthcare (Basel, Switzerland) · 2026Review
- Frailty and COPD: a bidirectional relationship in the context of systemic and accelerated ageing.European respiratory review : an official journal of the European Respiratory Society · 2026Review
- Sarcopenia in cognitive disorders: Toward a shared pathophysiological framework.Osteoporosis and sarcopenia · 2026Review
- Modulation of mitochondrial dysfunction: Mechanisms and strategies for the use of natural products to treat stroke.Neural regeneration research · 2026Article
- Electrophysiological Evaluation of Post-Activation Potentiation/Post-Activation Performance Enhancement Using Strength-Duration Properties.Journal of functional morphology and kinesiology · 2026Article
- Review
- CTRP1 regulates skeletal muscle differentiation through quality control of mitochondrial dynamics and function.Molecular therapy : the journal of the American Society of Gene Therapy · 2026Article
- Neuromuscular Junction as a Molecular Target in Sarcopenia: Mechanisms, Therapeutic Strategies, and Future Directions.Molecular diagnosis & therapy · 2026Review
- The Roles of myomiRs in the Pathogenesis of Sarcopenia: From Literature to In Silico Analysis.Molecular biotechnology · 2026Review
- The relationship between estimated glucose disposal rate and sarcopenia among middle-aged and older adults.Scientific reports · 2025Article
- Human Mesenchymal Stem Cell-Derived Skeletal Muscle Cell Spheroids for Treating Dexamethasone-Induced Sarcopenia.Tissue engineering and regenerative medicine · 2025Article
- PRMT1 (protein arginine methyltransferase 1) is essential for neuromuscular junction and mitochondrial homeostasis via mitophagy regulation.Autophagy · 2025Article
- Neural Cues and Genomic Clues: NGS Insights into Neurogenic Sarcopenia and Muscle Atrophy.International journal of molecular sciences · 2025Review
- Estrogens and Antioxidants Prevent the Formation of Tubular Aggregates in Aging Male Mice.International journal of molecular sciences · 2025Article
- Potential therapeutic role of sex steroids in treating sarcopenia: a network pharmacology and molecular dynamics study.BMC pharmacology & toxicology · 2025Article
- Mechanisms Underlying Muscle-Related Diseases and Aging: Insights into Pathophysiology and Therapeutic Strategies.Muscles (Basel, Switzerland) · 2025Review
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Sarcopenia is a systemic skeletal muscle disease characterized by a decline in skeletal muscle mass and function. Originally defined as an age-associated condition, sarcopenia presently also encompasses muscular atrophy due to various pathological factors, such as intensive care unit-acquired weakness, inactivity, and malnutrition. The exact pathogenesis of sarcopenia is still unknown; herein, we review the pathological roles of the neuromuscular junction and mitochondria in this condition. Sarcopenia is caused by complex and interdependent pathophysiological mechanisms, including aging, neuromuscular junction impairment, mitochondrial dysfunction, insulin resistance, lipotoxicity, endocrine factors, oxidative stress, and inflammation. Among these, neuromuscular junction instability and mitochondrial dysfunction are particularly significant. Dysfunction in neuromuscular junction can lead to muscle weakness or paralysis. Mitochondria, which are plentiful in neurons and muscle fibers, play an important role in neuromuscular junction transmission. Therefore, impairments in both mitochondria and neuromuscular junction may be one of the key pathophysiological mechanisms leading to sarcopenia. Moreover, this article explores the structural and functional alterations in the neuromuscular junction and mitochondria in sarcopenia, suggesting that a deeper understanding of these changes could provide valuable insights for the prevention or treatment of sarcopenia.
Indexed as
Identifiers
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.