Aged donor muscle-cell secretions and sphingolipids in stem-cell decline
In cell-culture experiments, secretions from muscle cells of aged donors (60–86 years) differed from young donors (15–25 years); the enzyme ASM was most increased and reduced PAX7+ stem cells, while S1P restored the stem-cell pool in aged cultures. [1]
Automatic summary · not editorially reviewed
The key findings
Proteomic and lipidomic analyses compared conditioned media from primary muscle cells of young (15–25 years) and aged (60–86 years) donors. [1]
Acid sphingomyelinase (ASM) was the most upregulated secreted factor, and recombinant ASM reduced PAX7+ muscle stem cells in young cultures. [1]
Exogenous S1P restored the stem-cell pool in aged cultures, and the authors name ASM and S1P as targets. [1]
The source at a glance
- Study type / format
- Abstract of a laboratory cell-culture study with proteomic and lipidomic analyses
- Population / context
- Primary muscle cells from young (15–25 years) and aged (60–86 years) human donors, studied in culture.
- Summary based on
- Study abstract
- Publication status
- Preprint · peer-review status not confirmed
- Original publication
- October 2, 2026
Secretions compared from young and aged donor muscle cells
The abstract notes that aging reduces skeletal muscle's ability to regenerate, but how the aged environment harms muscle stem cells (MuSCs) is unclear. Muscle is described as a secretory organ, yet age-related changes in what it secretes are poorly understood. To address this, the researchers analysed proteins and lipids in conditioned media from primary muscle cells of young donors (15–25 years) and aged donors (60–86 years).
Supporting source [1]
ASM up, sphingolipid axis disrupted, S1P restores stem cells
The analysis found 127 age-dependent secreted proteins, indicating major remodelling. The lysosomal enzyme acid sphingomyelinase (ASM), which converts sphingomyelin into ceramide, was the most upregulated factor. Recombinant ASM reduced PAX7+ MuSCs in young cultures, suggesting extracellular ASM impairs stem-cell maintenance. Lipid analysis showed disruption of the sphingomyelin–ceramide–S1P axis, with decreased sphingomyelin and S1P, a lipid that promotes MuSC proliferation. Exogenous S1P restored the stem-cell pool in aged cultures.
Supporting source [1]
Cell-culture findings only; abstract not full text
These results link secretome remodelling and sphingolipid metabolism to MuSC decline and name ASM and S1P as targets. However, the work was done in cell cultures from donor muscle cells, not in living people, so it does not show effects on human muscle regeneration or lifespan. The abstract does not report sample sizes, donor numbers or statistical details. This summary is based on the abstract only; the full text was not reviewed.
Supporting source [1]
How to interpret this
Abstract only; the full text was not reviewed. Findings come from cell-culture experiments with donor muscle cells, not from living humans, and sample sizes and statistical details are not reported in the abstract.
Based on the study abstract; the full paper, tables and supplementary data were not reviewed.
Source & supporting passages
Crisol B, Pinzón N, Bensalah M, Ohana J, Lhomme M, Ponnaiah M, Bruce J, Kondili M, Gaut L, Negroni E, Boulinguiez A, Butler-Browne G, Mouly V, Trollet C, Bigot A. · europepmc.org · October 2, 2026