ReviewCells2022
Adaptive Remodeling of the Neuromuscular Junction with Aging.
Review in Cells, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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, 47 citations in OpenAlex.
- Motor Cortex Hyperexcitability Is Coupled to Neuromuscular Dysfunction in Aged Mice.Aging cell · 2026Article
- Phytochemical-Based Therapeutic Strategies for Sarcopenia: From Molecular Mechanisms to Clinical Translation.Pharmaceuticals (Basel, Switzerland) · 2026Review
- Mechanisms and precision interventions in sarcopenia and osteoarthritis comorbidity: A narrative review.Journal of orthopaedic translation · 2026Review
- Article
- Review
- Aging induces sarcopenia by disrupting the crosstalk between the skeletal muscle microenvironment and myofibers.Journal of advanced research · 2026Review
- Neuromuscular junction instability with inactivity: morphological and functional changes after 10 days of bed rest in older adults.The Journal of physiology · 2026Article
- Sarcopenia in the Aging Process: Pathophysiological Mechanisms, Clinical Implications, and Emerging Therapeutic Approaches.International journal of molecular sciences · 2025Review
- Donepezil treatment, alone or combined with exercise, enhances skeletal muscle function in healthy and advanced aging disease mouse models.Journal of applied physiology (Bethesda, Md. : 1985) · 2025Article
- A role for the transcriptional coregulator RIP140 in the control of muscle endurance fitness.JCI insight · 2025Article
- Cell and tissue reprogramming: Unlocking a new era in medical drug discovery.Pharmacological reviews · 2025Review
- Mesenchymal Stromal Cell-Derived Extracellular Vesicles as a Therapeutic Treatment for Osteosarcopenia: Crosstalk Among Neurons, Muscle, and Bone.International journal of molecular sciences · 2025Article
- HDAC11 deficiency regulates age-related muscle decline and sarcopenia.GeroScience · 2025Article
- Mature and Juvenile Neuromuscular Plasticity in Response to Unloading.Developmental neurobiology · 2025Article
- Why Dosing Matters: A Closer Look at the Dose-Response Relationship With OnabotulinumtoxinA.Journal of cosmetic dermatology · 2025Review
- Age, cancer, and the dual burden of cancer and doxorubicin in skeletal muscle wasting in female rats: which one to blame?Biogerontology · 2025Article
- Sarcopenia and Cardiogeriatrics: The Links Between Skeletal Muscle Decline and Cardiovascular Aging.Nutrients · 2025Review
- Impact of exercise-induced DNA damage repair on age-related muscle weakness and sarcopenia.Frontiers in genetics · 2025Review
- In vivo AAV9-Myo7a gene rescue restores hearing and cholinergic efferent innervation in inner hair cells.JCI insight · 2024Article
- Functional and Structural Changes in Diaphragm Neuromuscular Junctions in Early Aging.International journal of molecular sciences · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Aging is associated with gradual degeneration, in mass and function, of the neuromuscular system. This process, referred to as "sarcopenia", is considered a disease by itself, and it has been linked to a number of other serious maladies such as type II diabetes, osteoporosis, arthritis, cardiovascular disease, and even dementia. While the molecular causes of sarcopenia remain to be fully elucidated, recent findings have implicated the neuromuscular junction (NMJ) as being an important locus in the development and progression of that malady. This synapse, which connects motor neurons to the muscle fibers that they innervate, has been found to degenerate with age, contributing both to senescent-related declines in muscle mass and function. The NMJ also shows plasticity in response to a number of neuromuscular diseases such as amyotrophic lateral sclerosis (ALS) and Lambert-Eaton myasthenic syndrome (LEMS). Here, the structural and functional degradation of the NMJ associated with aging and disease is described, along with the measures that might be taken to effectively mitigate, if not fully prevent, that degeneration.
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.