Senescent-like USS-high muscle stem cells and S1P in mouse muscle regeneration
In an abstract on acutely injured mouse muscle, a USS-high muscle stem cell subpopulation with senescent-like features secreted S1P; ablating it impaired regeneration, and exogenous S1P rescued that deficit. [1]
Automatic summary · not editorially reviewed
The key findings
A USS-high MuSC subpopulation with senescent-like features appeared early in injury-induced mouse muscle regeneration and secreted pro-inflammatory factors and S1P. [1]
Genetic ablation of this subpopulation significantly impaired muscle regeneration in vivo. [1]
Exogenous S1P rescued the regenerative deficits caused by ablating USS-high MuSCs. [1]
The source at a glance
- Study type / format
- Preclinical multiomics study in mice (abstract)
- Population / context
- Acutely injured skeletal muscle in mice
- Summary based on
- Study abstract
- Publication status
- Preprint · peer-review status not confirmed
- Original publication
- September 22, 2026
USS-high MuSCs in early mouse injury repair
The abstract describes single-cell RNA sequencing with a Unified Senescence Score (USS) in acutely injured mouse skeletal muscle. A distinct USS-high muscle stem cell (MuSC) subpopulation appeared in the early phase of injury-induced regeneration. Isolated via the surface marker MHCII, these cells showed canonical senescent-like features. Integrated transcriptomics, proteomics and secretomics indicated a strongly pro-inflammatory secretory capacity, and lipidomic profiling showed sphingolipid remodeling that raised the bioactive lipid sphingosine-1-phosphate (S1P).
Supporting source [1]
Ablation impairs repair; S1P rescues in mice
In vivo, specific ablation of this subpopulation using a Pax7-CreERT; Ccl2-LSL-DTA genetic strategy significantly impaired muscle regeneration. Spatial transcriptomics and cell-cell communication analyses indicated that USS-high MuSCs act as niche modulators, directing crosstalk with multiple cell types. S1P was reported as essential for direct interaction of USS-high cells with endothelial cells and USS-low cells, promoting endothelial angiogenesis and MuSC expansion in regenerating muscle. Exogenous S1P rescued the regenerative deficits caused by ablation of USS-high MuSCs.
Supporting source [1]
Abstract-only mouse evidence, not human lifespan data
These findings concern acutely injured mouse skeletal muscle and a senescent-like MuSC population; they describe regeneration, not lifespan or human outcomes. The abstract does not report sample sizes, follow-up duration or detailed statistics, and the full text was not reviewed. The results are associations and experimental interventions in animals, not proof that the same cells or S1P would benefit people.
Supporting source [1]
How to interpret this
Abstract only; the full text was not reviewed. Mouse injury model; no sample sizes, follow-up or detailed statistics reported. Findings concern muscle regeneration, not human lifespan.
Based on the study abstract; the full paper, tables and supplementary data were not reviewed.
Source & supporting passages
Liu X, Zhang Y, Li Y, Jin Y, Qiao Y, Li C, Wang S, Lam SM, Shui G, Wong CC, Sun H, Kuang S, Wang H. · europepmc.org · September 22, 2026