Evidence map›Paper›PMID 40932671›Full record

ArticleNeurochemical research2025

Cholesterol-Lowering Treatment Suppresses Neuromuscular Transmission Via Presynaptic Mechanism at the Mouse Diaphragm Muscle.

Guzel F Zakyrjanova, Andrei N Tsentsevitsky, Valeriya A Matigorova, Nikita S Fedorov, Julia G Odnoshivkina, Guzel V Sibgatullina, Eva A Kapliukhina, Arthur R Giniatullin, Arthur N Khaziev, Artem I Malomouzh and 2 more

Abstract read
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Article in Neurochemical research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing 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

4 citing papers in PubMed.

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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

12 authors.

Guzel F ZakyrjanovaLaboratory of Biophysics of Synaptic Processes, Kazan Institute of Biochemistry and Biophysics, Federal Research Center - Kazan Scientific Center of RAS, 2/31 Lobachevsky Street, Kazan, 420111, Russia.
Andrei N TsentsevitskyLaboratory of Biophysics of Synaptic Processes, Kazan Institute of Biochemistry and Biophysics, Federal Research Center - Kazan Scientific Center of RAS, 2/31 Lobachevsky Street, Kazan, 420111, Russia.
Valeriya A MatigorovaLaboratory of Biophysics of Synaptic Processes, Kazan Institute of Biochemistry and Biophysics, Federal Research Center - Kazan Scientific Center of RAS, 2/31 Lobachevsky Street, Kazan, 420111, Russia.
Nikita S FedorovLaboratory of Biophysics of Synaptic Processes, Kazan Institute of Biochemistry and Biophysics, Federal Research Center - Kazan Scientific Center of RAS, 2/31 Lobachevsky Street, Kazan, 420111, Russia.
Julia G OdnoshivkinaLaboratory of Biophysics of Synaptic Processes, Kazan Institute of Biochemistry and Biophysics, Federal Research Center - Kazan Scientific Center of RAS, 2/31 Lobachevsky Street, Kazan, 420111, Russia.
Guzel V SibgatullinaLaboratory of Biophysics of Synaptic Processes, Kazan Institute of Biochemistry and Biophysics, Federal Research Center - Kazan Scientific Center of RAS, 2/31 Lobachevsky Street, Kazan, 420111, Russia.
Eva A KapliukhinaLaboratory of Biophysics of Synaptic Processes, Kazan Institute of Biochemistry and Biophysics, Federal Research Center - Kazan Scientific Center of RAS, 2/31 Lobachevsky Street, Kazan, 420111, Russia.
Arthur R GiniatullinDepartment of Normal Physiology, Institute of Neuroscience, Kazan State Medical University, 49 Butlerova Street, Kazan, 420012, Russia.
Arthur N KhazievLaboratory of Biophysics of Synaptic Processes, Kazan Institute of Biochemistry and Biophysics, Federal Research Center - Kazan Scientific Center of RAS, 2/31 Lobachevsky Street, Kazan, 420111, Russia.
Artem I MalomouzhLaboratory of Biophysics of Synaptic Processes, Kazan Institute of Biochemistry and Biophysics, Federal Research Center - Kazan Scientific Center of RAS, 2/31 Lobachevsky Street, Kazan, 420111, Russia.
Yuri V GogolevLaboratory of Biophysics of Synaptic Processes, Kazan Institute of Biochemistry and Biophysics, Federal Research Center - Kazan Scientific Center of RAS, 2/31 Lobachevsky Street, Kazan, 420111, Russia.
Alexey M PetrovLaboratory of Biophysics of Synaptic Processes, Kazan Institute of Biochemistry and Biophysics, Federal Research Center - Kazan Scientific Center of RAS, 2/31 Lobachevsky Street, Kazan, 420111, Russia. alexey.petrov@kazangmu.ru.

Funding

Russian Science Foundation 23-15-00124Russian Science Foundation 23-75-10022
6 · The paper itself

Abstract

Statins are widely prescribed and effective cholesterol-lowering drugs for the therapy of cerebrovascular and cardiovascular disorders. The main side effects limiting statin use are muscle-related adverse events, including weakness and myopathy. The precise mechanisms of statin-induced muscle damage remain to be elucidated. Possible alterations in neuromuscular transmission might contribute to the statin side effects. Here, we studied the action of one-month treatment with atorvastatin, the most prescribed statin, on the functioning of neuromuscular junctions and related processes in the mouse diaphragm. We found that atorvastatin treatment decreases evoked acetylcholine (ACh) release and involvement of synaptic vesicles in exocytosis during intense nerve activation, as well as recovery of ACh release after tetanic stimulation. This was accompanied by increased immunolabeling of synapsin 1, a protein retaining synaptic vesicles in a non-active pool, and decreased non-quantal ACh release under resting conditions. Additionally, atorvastatin administration decreased perimeters of postsynaptic ACh receptor clusters without signs of muscle denervation. Diaphragm contractile responses to phrenic nerve stimulation at moderate-to-high frequencies and peak inspiratory flow, an indicator of diaphragm function in vivo, were decreased in atorvastatin-treated mice, whereas diaphragm contractions elicited by direct stimulation of muscle fibers were unchanged. Thus, atorvastatin treatment caused a decline in evoked ACh release and synaptic vesicle recruitment into neurotransmission that could lead to a reduction of diaphragm contractile responses to phrenic nerve activity and peak inspiratory flow. These alterations, in combination with decreased non-quantal ACh release and neuromuscular junction size, may contribute to statin-associated muscle symptoms.

Indexed as

Anticholesteremic AgentsAtorvastatinDiaphragmNeuromuscular JunctionSynaptic TransmissionAcetylcholineAnimalsMaleMiceMice, Inbred C57BLMuscle ContractionPhrenic NerveSynaptic VesiclesAcetylcholineAnticholesteremic AgentsAtorvastatinAtorvastatinExocytosisMuscle contractionNeuromuscular junctionNeurotransmitter releaseStatin-associated muscle symptoms

Identifiers

PMID40932671

What Socratic holds

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Registered trials

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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 Socratic graph.