ArticleFrontiers in pharmacology2022
Dexmedetomidine inhibits abnormal muscle hypertrophy of myofascial trigger points
Article in Frontiers in pharmacology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 5 citations in OpenAlex.
- A Time-Efficient and Reproducible Rat Model of Myofascial Pain Syndrome-Like Phenotypes Induced by Repeated Mechanical Impact and Eccentric Exercise.Journal of pain research · 2026Article
- Article
- PDGFR-α Mediated the Neuroinflammation and Autophagy via the JAK2/STAT3 Signaling Pathway Contributing to Depression-Like Behaviors in Myofascial Pain Syndrome Rats.Molecular neurobiology · 2025Article
- The Mechanism of α2 adrenoreceptor-dependent Modulation of Neurotransmitter Release at the Neuromuscular Junctions.Neurochemical research · 2024Article
- Article
Corrections and comments
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Authors and funding
6 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Myofascial pain syndrome (MPS) is a chronic pain disorder with inflammation-related primarily characterized by the presence of myofascial trigger points (MTrPs). Myocyte enhancer factor 2C (MEF2C) is involved in the occurrence of a variety of skeletal muscle diseases. However, it is not yet clear if MEF2C is involved in MTrPs. The purpose of this study was to investigate whether MEF2C was involved in the inflammatory pathogenesis of MTrPs. In the present study, we used RNA sequencing (RNA-seq) to compare the differential expression of myocyte enhancer factor 2C (MEF2C) in healthy participants and MTrPs participants. The widely used rat MTrPs model was established to research the upstream and downstream regulatory mechanism of MEF2C and found that MEF2C was significantly increased in patients with MTrPs. Dexmedetomidine (Dex) was injected intramuscularly in the MTrPs animal to assess its effects on MEF2C. The expression of MEF2C protein and mRNA in skeletal muscle of rats in the MTrPs group were up-regulated. In addition, the expression of TNF- α, p-P65, MLCK, and Myocilin (MyoC) was up-regulated and the mechanical pain threshold was decreased. Peripheral TNF-
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