Evidence map›Paper›PMID 41388353›Full record

ArticleOral diseases2026

Mitophagy in Botulinum Toxin Type A-Induced Muscle Atrophy.

Qian-Ying Mao, Zhuo Chen, Shang Xie, Ruo-Lan Xiang, Zhi-Gang Cai

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Oral diseases, 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

5 authors.

Qian-Ying MaoDepartment of Oral and Maxillofacial Surgery, Peking University School and Hospital of Stomatology & National Center for Stomatology & National Clinical Research Center for Oral Diseases & National Engineering Research Center of Oral Biomaterials and Digital Medical Devices, Beijing, China.
Zhuo ChenDepartment of Physiology and Pathophysiology, Peking University School of Basic Medical Sciences, Key Laboratory of Molecular Cardiovascular Sciences, Ministry of Education, Beijing, China.
Shang XieDepartment of Oral and Maxillofacial Surgery, Peking University School and Hospital of Stomatology & National Center for Stomatology & National Clinical Research Center for Oral Diseases & National Engineering Research Center of Oral Biomaterials and Digital Medical Devices, Beijing, China.
Ruo-Lan XiangDepartment of Physiology and Pathophysiology, Peking University School of Basic Medical Sciences, Key Laboratory of Molecular Cardiovascular Sciences, Ministry of Education, Beijing, China.ORCID https://orcid.org/0000-0001-5935-1911
Zhi-Gang CaiDepartment of Oral and Maxillofacial Surgery, Peking University School and Hospital of Stomatology & National Center for Stomatology & National Clinical Research Center for Oral Diseases & National Engineering Research Center of Oral Biomaterials and Digital Medical Devices, Beijing, China.ORCID https://orcid.org/0000-0001-7657-8843

Funding

National Natural Science Foundation of China 82470994
6 · The paper itself

Abstract

objectiveBotulinum toxin type A (BTXA) is widely used in oral and maxillofacial surgery to treat masseter hypertrophy and bruxism, inducing transient masseter atrophy, but the underlying mechanisms remain unclear. Mitophagy, essential for muscle fiber homeostasis, plays a critical role in muscle atrophy. This study aims to investigate whether mitophagy mediates BTXA-induced masseter muscle atrophy.

methodsRats received BTXA injections into masseter for 2 and 8 weeks. Muscle fiber composition was assessed via histology and immunofluorescence. Mitophagy markers (LC3-II, p62, beclin-1, Tomm20) were quantified by western blot. Mitochondrial function was evaluated via ATP content and mitochondrial DNA (mtDNA) copy number.

resultsBTXA injection led to transient masseter muscle atrophy. During this process, the proportion of type IIA muscle fibers significantly increased, while the proportion of type IIB fibers decreased. Additionally, at 2 weeks post-BTXA injection, the expression levels of LC3-II, p62, and beclin-1 were notably upregulated, whereas Tomm20 expression was downregulated. Furthermore, a significant reduction in ATP content and mtDNA copy number was observed at the same time point, indicating impaired mitochondrial function.

conclusionThese findings suggest that mitophagy plays a crucial role in BTXA-induced masseter muscle atrophy, providing new insights into the mechanisms underlying BTXA treatment.

Indexed as

Botulinum Toxins, Type AMasseter MuscleMitophagyMuscular AtrophyAdenosine TriphosphateAnimalsBeclin-1DNA, MitochondrialMaleMembrane Transport ProteinsMicrotubule-Associated ProteinsMitochondrial Precursor Protein Import Complex ProteinsRatsRats, Sprague-DawleyAdenosine TriphosphateAnxa3 protein, ratBeclin-1Becn1 protein, ratBotulinum Toxins, Type ADNA, MitochondrialMembrane Transport ProteinsMicrotubule-Associated ProteinsMitochondrial Precursor Protein Import Complex Proteinsbotulinum toxin type Amasseter musclemitophagymuscle atrophy

Identifiers

PMID41388353
PMCPMC13364994

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.