Mouse and cell study: olfactory receptor OR10J5 and skeletal muscle aging
In this abstract, the olfactory receptor OR10J5 was linked to skeletal muscle senescence and aging in cells and mice; activating it with lyral improved muscle measures in naturally aged wild-type mice but not in mice lacking Or10j5. [1]
Automatic summary · not editorially reviewed
The key findings
Or10j5 mRNA expression was reduced in cellular senescence and atrophy models, mouse atrophy models and naturally aged skeletal muscle. [1]
Genetic ablation of Or10j5 exacerbated age-associated muscle loss and functional decline in mice. [1]
Lyral improved muscle mass and physical performance in naturally aged wild-type mice but not in Or10j5-deficient mice. [1]
The source at a glance
- Study type / format
- Preclinical study reported in an abstract (cell models and mice)
- Population / context
- Cellular senescence and muscle atrophy models, mouse models of muscle atrophy, naturally aged mice, Or10j5-deficient mice and human embryonic stem cell-derived myotubes.
- Summary based on
- Study abstract
- Publication status
- Preprint · peer-review status not confirmed
- Original publication
- September 21, 2026
Reduced Or10j5 across senescence and atrophy models
The abstract reports that Or10j5 mRNA expression was reduced in cellular models of senescence and muscle atrophy, in mouse models of muscle atrophy, and in naturally aged skeletal muscle. The authors describe OR10J5 as an ectopic olfactory receptor and a regulator of skeletal muscle senescence and aging. These are expression observations across models, not evidence that low Or10j5 causes human muscle aging.
Supporting source [1]
Ablation worsened, lyral improved aged mouse muscle
Genetic ablation of Or10j5 exacerbated age-associated muscle loss and functional decline in mice, with increased senescence-associated changes. Conversely, pharmacological activation of OR10J5 with lyral attenuated senescence- and atrophy-associated phenotypes and improved muscle mass and physical performance in naturally aged wild-type mice, but not in Or10j5-deficient mice. Lyral also attenuated these phenotypes in human embryonic stem cell-derived myotubes. The abstract does not report sample sizes, effect sizes or how long the mice were followed.
Supporting source [1]
Proposed signaling route and stated limits
Mechanistically, the abstract states that lyral activates OR10J5-dependent cAMP-PKA-CREB signaling and modulates transcriptional programs related to myogenesis, mitochondrial biogenesis and cellular senescence. The authors conclude that OR10J5 activation is a potential strategy to counter age-related muscle decline. This is a proposed strategy from preclinical cell and mouse work, not a demonstrated benefit for human muscle aging. Only the abstract was reviewed; the full text was not reviewed.
Supporting source [1]
How to interpret this
Abstract only; the full text was not reviewed. Sample sizes, effect sizes, follow-up and detailed methods are not reported in the abstract. Findings come from cell models and mice, so they do not establish benefit for human muscle aging.
Based on the study abstract; the full paper, tables and supplementary data were not reviewed.
Source & supporting passages
Suh Y, Kim J, Yang J, Lee Y, Choi S, Shin S, Hwang C, Lee Y, Cho S, Han H, Yoon Y, Lee HS, Scheibye-Knudsen M, Lee S. · europepmc.org · September 21, 2026