Chick muscle cells treated with Ara-C as an in vitro senescence model
In cultured embryonic chick muscle cells, nine days of low-dose Ara-C produced several senescence-associated features and reduced muscle differentiation; blocking the fibroblast growth factor receptor reversed the phenotype in myogenic cells. [1]
Automatic summary · not editorially reviewed
The key findings
Cultured embryonic chick muscle cells received a low concentration of cytosine arabinoside (Ara-C) for nine days to induce cell cycle arrest. [1]
Ara-C treatment was associated with reduced cell proliferation, increased β-galactosidase, more reactive oxygen species, higher p53 and p21, larger muscle fibroblast cells with more nuclei, increased lysosomal activity, decreased muscle fiber size and desmin, and increased secretion of IL-6, TNFα and TGFβ. [1]
Inhibiting the fibroblast growth factor receptor recovered the Ara-C-induced senescent phenotype in myogenic cells. [1]
The source at a glance
- Study type / format
- In vitro primary cell culture study (abstract).
- Population / context
- Cultured embryonic chick skeletal muscle cells.
- Summary based on
- Study abstract
- Original publication
- September 18, 2026
Ara-C in embryonic chick muscle cell culture
The authors aimed to build a primary cell culture model for skeletal muscle cell senescence. They used cultured embryonic chick muscle cells and induced cell cycle arrest with a low concentration of cytosine arabinoside (Ara-C) for nine days. This is a laboratory cell model, not a study of people or of lifespan.
Supporting source [1]
Senescence features and weaker muscle differentiation
Ara-C induced several senescence-associated characteristics: reduced cell proliferation, increased β-galactosidase expression, more reactive oxygen species, higher p53 and p21 expression, larger muscle fibroblast cell size with more nuclei, and increased lysosomal activity. Muscle differentiation decreased, shown by smaller muscle fibers and lower desmin expression. Secretion of IL-6, TNFα and TGFβ increased. These are measured associations in this model, not proof of cause in human aging.
Supporting source [1]
Receptor blockade and proposed model uses
Inhibiting the fibroblast growth factor receptor recovered the Ara-C-induced senescent phenotype in myogenic cells. The authors conclude that this new experimental model could help clarify molecules and signaling pathways involved in the initiation and establishment of skeletal muscle senescence. They also suggest it could be used to test drugs and therapeutic interventions aimed at senescence-associated conditions. These are proposed uses, not demonstrated treatments.
Supporting source [1]
How to interpret this
Abstract only; the full text was not reviewed. This is an in vitro embryonic chick cell model, so the findings do not establish effects in humans, in adult muscle or on lifespan. Proposed drug-testing uses are not validated treatments.
Based on the study abstract; the full paper, tables and supplementary data were not reviewed.
Source & supporting passages
Bagri KM, Lima Castelo-Branco MT, Mermelstein C. · europepmc.org · September 18, 2026