ArticleBMC medical genomics2023
A link between mitochondrial damage and the immune microenvironment of delayed onset muscle soreness.
Article in BMC medical genomics, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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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.
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Who cites it
4 citing papers in PubMed, 4 citations in OpenAlex.
- Deciphering the action mechanism of the sacred plant "Ashvattha" (Ficus religiosa L.) in the treatment of delayed-onset muscle soreness.Journal of Ayurveda and integrative medicine · 2026Article
- Piezo2-Initiated Ultrafast Signaling and Its Acquired Channelopathy in Light of Quantum Gravity Theory.International journal of molecular sciences · 2026Review
- Delayed-Onset Muscle Soreness Begins with a Transient Neural Switch.International journal of molecular sciences · 2025Review
- Review
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundDelayed onset muscle soreness (DOMS) is a self-healing muscle pain disorder. Inflammatory pain is the main feature of DOMS. More and more researchers have realized that changes in mitochondrial morphology are related to pain. However, the role of mitochondria in the pathogenesis of DOMS and the abnormal immune microenvironment is still unknown.
methodsMitochondria-related genes and gene expression data were obtained from MitoCarta3.0 and NCBI GEO databases. The network of mitochondrial function and the immune microenvironment of DOMS was constructed by computer algorithm. Subsequently, the skeletal muscle of DOMS rats was subjected to qPCR to verify the bioinformatics results. DOMS and non-DOMS histological samples were further studied by staining and transmission electron microscopy.
resultsBioinformatics results showed that expression of mitochondria-related genes was changed in DOMS. The results of qPCR showed that four hub genes (AMPK, PGC1-α, SLC25A25, and ARMCX1) were differentially expressed in DOMS. These hub genes are related to the degree of skeletal muscle immune cell infiltration, mitochondrial respiratory chain complex, DAMPs, the TCA cycle, and mitochondrial metabolism. Bayesian network inference showed that IL-6 and PGC1-α may be the main regulatory genes of mitochondrial damage in DOMS. Transmission electron microscopy revealed swelling of skeletal muscle mitochondria and disorganization of myofilaments.
conclusionsOur study found that skeletal muscle mitochondrial damage is one of the causes of inflammatory factor accumulation in DOMS. According to the screened-out hub genes, this study provides a reference for follow-up clinical application.
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