Evidence map›Paper›PMID 41619083›Full record

ReviewMolecular diagnosis & therapy2026

Neuromuscular Junction as a Molecular Target in Sarcopenia: Mechanisms, Therapeutic Strategies, and Future Directions.

Rizwan Qaisar, Firdos Ahmad, Asima Karim

Abstract readReview
PubMed Publisher
In one paragraph

Review in Molecular diagnosis & therapy, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from 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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors.

Rizwan QaisarDepartment of Basic Medical Sciences, College of Medicine, University of Sharjah, 27272, Sharjah, United Arab Emirates. rqaisar@sharjah.ac.ae.ORCID 0000-0001-8485-7172
Firdos AhmadDepartment of Basic Medical Sciences, College of Medicine, University of Sharjah, 27272, Sharjah, United Arab Emirates.
Asima KarimDepartment of Basic Medical Sciences, College of Medicine, University of Sharjah, 27272, Sharjah, United Arab Emirates.

Funding

University of Sharjah 25010901180
6 · The paper itself

Abstract

Sarcopenia is a progressive loss of skeletal muscle mass and strength that significantly contributes to frailty and disability in older adults. Traditionally considered a consequence of myofiber atrophy and impaired protein turnover, recent evidence highlights neuromuscular junction (NMJ) degeneration as an early and critical event in the pathogenesis of this condition. Structural and functional changes at the NMJ, including fragmentation of acetylcholine receptor clusters, motor neuron loss, and disruption of agrin-muscle-specific kinase (MuSK) signaling, impair neuromuscular transmission and accelerate muscle decline. This review synthesizes current understanding of NMJ biology, its age-related deterioration, and emerging therapeutic strategies aimed at preserving synaptic integrity. We discuss pharmacological approaches that target presynaptic neurotransmitter synthesis, stabilize the synaptic cleft, and enhance postsynaptic receptor clustering, as well as interventions that activate Schwann and satellite cells to restore regenerative capacity. Adjunctive therapies such as antioxidants, mitochondrial protectants, and metabolic modulators complement NMJ-specific drugs by mitigating oxidative stress and inflammation. Translational insights underscore the importance of NMJ-specific biomarkers, such as circulating c-terminal agrin fragment-22 (CAF22), and advanced imaging modalities to facilitate early detection and personalized interventions. Future directions focus on multimodal regimens that combine NMJ-targeted agents with exercise, nutrition, and digital health tools, supported by computational analytics for precision care. By integrating molecular, systemic, and lifestyle strategies, NMJ-focused therapies offer a promising approach to delaying the progression of sarcopenia and improving functional independence in aging populations. Continued interdisciplinary research and mechanistically informed clinical trials are crucial for translating these advances into effective treatments.

Indexed as

Neuromuscular JunctionSarcopeniaAnimalsHumansMolecular Targeted TherapyReceptor Protein-Tyrosine KinasesReceptors, CholinergicReceptor Protein-Tyrosine KinasesReceptors, Cholinergic

Identifiers

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.