ArticleAging2022
C-C motif chemokine ligand 2 promotes myogenesis of myoblasts via the AKT-mTOR pathway.
Article in Aging, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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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.
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.
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Who cites it
7 citing papers in PubMed, 10 citations in OpenAlex.
- Review
- Modulating iMSC Spheroid Function with Mechanically Tunable Hydrogels to Strengthen the Bone-Muscle Axis.ACS biomaterials science & engineering · 2026Article
- CXCL14 Promotes Skeletal Muscle Mass Growth and Attenuates Lipopolysaccharide- and Dexamethasone-Induced Muscle Atrophy in Cultured Myotubes and Mouse Models.Journal of cachexia, sarcopenia and muscle · 2025Article
- Transcriptome Analysis of Differentially Expressed Genes and Molecular Pathways Involved in C2C12 Cells Myogenic Differentiation.Molecular biotechnology · 2025Article
- Nanoparticle-Driven Skeletal Muscle Repair and Regeneration Through Macrophage-Muscle Stem Cell Interaction.Small (Weinheim an der Bergstrasse, Germany) · 2025Article
- Review
- Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Muscle mass decreases with aging, while the C-C motif chemokine ligand 2 (CCL2) increases with aging; in this context, CCL2 can be considered a potential aging-promoting factor. Thus, CCL2 knockout mice are expected to exhibit anti-aging effects including protection against loss of muscle mass. However, instead, muscle amount and recovery of damaged muscles are decreased in CCL2 knockout mice. Therefore, we hypothesized that increasing CCL2 in the elderly might be related to compensation for loss of muscle mass. To confirm the relationship between muscle and CCL2, we sought to establish the role of CCL2 in C2C12 cells and Human Skeletal Muscle Myoblast (HSMM) cells. The myotube (MT) fusion index increased with CCL2 compared to 5day CCL2 vehicle only (27.0 % increase, P<0.05) in immunocytochemistry staining (ICC) data. CCL2 also restored MTs atrophy caused by dexamethasone (21.8 % increase, P<0.0001). p-mTOR/mTOR and p-AKT/total AKT increased with CCL2 compared to CCL2 vehicle only (18.3 and 30.5% increase respectively, P<0.05) and decreased with CCR2-siRNA compared to CCL2 (38.9 % (P<0.05) and 56.7% (P<0.005) reduction respectively). In conclusion, CCL2 positively affects myogenesis by CCR2 via AKT-mTOR signaling pathways. CCL2 might have potential as a therapeutic target for low muscle mass and muscle recovery.
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Registered trials
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.